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. 2009 Apr 14;2009:bcr09.2008.0893. doi: 10.1136/bcr.09.2008.0893

A patient with Legionnaires’ disease transferred after a traffic accident

Ryota Sakamoto 1, Akira Ohno 2, Toshitaka Nakahara 1, Kazunari Satomura 1, Suketaka Iwanaga 1, Masahiko Saito 3, Kiyohito Okumiya 4, Keizo Yamaguchi 2
PMCID: PMC3027615  PMID: 21686578

Abstract

Legionnaires’ disease (LD) ranks among the three most common causes of severe pneumonia, but is often not specifically diagnosed. Among patients with LD, 40% to 50% of the patients develop neuromuscular signs and symptoms. A patient with LD transferred to our department after a traffic accident. When the patient arrived at our hospital, his respiratory rate was 27 breaths per min. His pulse was 148 beats per min and blood pressure was 116/57 mm Hg. Temperature was 39.6°C. He had copious watery diarrhoea and had been diagnosed as having acute gastroenteritis. The patient had urinary incontinence, gait disturbance, mild headache, fatigue and excessive decrease in spontaneous speech. A urinary antigen test for Legionella pneumophila turned out to be positive. LD commonly involves the neuromuscular system. Although this may be an atypical case of LD, it implies the need for awareness of LD.

BACKGROUND

Legionnaires’ disease (LD) accounts for 2% to 15% of all community-acquired pneumonias that require hospitalisation and ranks among the three most common causes of severe pneumonia.1 Although all cases must be reported to local health agencies, only about 0.5 cases per 100 000 population with LD were reported annually in Japan in 2006. These data imply that about 13 times the actual number of reported patients with LD are either undiagnosed or unreported in Japan. The number has been doubling with the use of urinary antigen test kits. In patients with LD, 40% to 50% of the patients develop neuromuscular signs and symptoms including headache, confusion, personal changes, ataxia, hallucinations, dysarthria, memory loss, urinary incontinence, myalgia, weakness, somnolence, inattentiveness and so on.28 As far as we know there has been no work in the literature to date to suggest the possibility that LD can trigger traffic accidents, although patients with LD often show neuromuscular signs and symptoms.

CASE PRESENTATION

A 54-year-old man was transferred to the Emergency Department (ED) via Emergency Medical Services (EMS) from a truck accident in the rainy season. When the patient arrived at our hospital, his respiratory rate was 27 breaths/min, pulse was 148 beats/min and blood pressure was 116/57 mm Hg. Oxygen saturation was 90% while he was breathing ambient air, and temperature was 39.6°C. Right lower lobe rales were noted on chest auscultation. The patient was responsive to questioning but had an excessive decrease in spontaneous speech. A serious bruise was not found. There had been copious watery diarrhoea 3–4 times per day for the last 4 days, as well as fever, shortness of breath and excessive fatigue. He had an excessive decrease in spontaneous speech, urinary incontinence and mild headache. Other results of the neurological examination were unremarkable. He did not have cough, chest pain or abdominal pain. He denied recent contact with sick persons or travel. He also denied exposure to a hot spring spa, a bath with a constant circulation system, or a cooling tower or a fountain. He had visited a general practice doctor 3 days before and had been diagnosed as having acute gastroenteritis. A chest radiograph showed right lower lobe pneumonia (fig 1). Sputum Gram stain showed neutrophils and few microbes. The patient was a commercial truck driver who consumed alcoholic drinks almost every day and had a 60 packs/year history of tobacco use. HIV test was negative. Emergency department laboratory values were leukocytes 13.6×103/μl with 83.5% segmented neutrophils and 11.5% stab cells, haemoglobin 14.0 g/dl, Na 117 mEq/litre, K 3.3 mEq/litre, blood urea nitrogen 24.1 mg/dl, creatinine 1.2 mg/dl, creatine phosphokinase 8231 U/litre, P 2.2 mg/dl and C-reactive protein 30.8 mg/dl. Liver enzymes showed alanine aminotransferase 462 U/litre and aspartate aminotransferase 229 U/litre. Arterial blood gas valued obtained on inspired room air showed pH 7.533, pCO2 22.6 mm Hg, pO2 54.0 mm Hg and HCO3 18.9 mmol/litre. Urinalysis showed 1–4 leukocytes and positive occult blood test.

Figure 1.

Figure 1

A chest CT scan showing consolidation in the right lower lobe of lung.

INVESTIGATIONS

Legionella spp. was not isolated from repeatedly submitted sputum specimens of buffered charcoal yeast extract agar (BCYE). Urinary antigen test for Legionella pneumophila turned out to be positive.

TREATMENT

Ciprofloxacin was administrated.

OUTCOME AND FOLLOW-UP

In the course of hospitalisation, the number of words the patient could speak increased and he informed us that he failed to negotiate a curve and went ogg of the road when he had the accident. Although he had a gait disturbance during the process of recovery, it was completely resolved within a month and the patient has resumed his normal life.

DISCUSSION

A patient with unstable vital signs transferred to the ED from a crash scene turned out to be positive for LD. Although we could not find other similar cases through a review of the literature, there undoubtably would have been and will be such cases. LD constitutes a large part of pneumonia cases and is often accompanied by various neuromuscular manifestations such as encephalomyelitis, cerebellar involvement, peripheral neuropathy, myositis and so on.911 The pathogenic mechanism of Legionella-induced neuromuscular dysfunction is unknown. Despite frequent neurological manifestations, neuroimaging studies are often normal and neuropathological studies often have failed to demonstrate bacilli or lesions attributable to invasion of neuromuscular system by Legionella. The production of a toxin by the bacillus or immune-mediated mechanisms has been suggested as a possible explanation of neuromuscular involvements in several reports.

According to the patient and the ambulance crews, the patient seems to have failed to negotiate a curve and deviated off the road. He may have had inattentiveness, steered in the wrong direction, or pressed on the brake too weakly because he had severe fatigue. There is an intriguing report of a patient with LD who had similar symptoms to our case. Morgan et al found a transient lesion in the splenium of the corpus callosum on brain MRI from a patient who had somnolence, inattentiveness, gait disturbance and word-finding difficulty, which was completely resolved 13 days later.12 Kashiwagi et al described a patient who demonstrated left neglect signs after callosal infarction.13 These are only a matter of speculation, but there is a possibility that he had such a lesion at the callosum causing left spatial neglect and so deviated to the left.

LEARNING POINTS

  • Legionnaires’ disease is one of the major causes of pneumonia, especially of severe pneumonia.

  • Legionnaires’ disease commonly involves the neuromuscular system.

  • Legionnaires’ disease is sometimes misdiagnosed as acute gastroenteritis because of copious watery diarrhoea.

Acknowledgments

We acknowledge the advice of Kozo Matsubayashi, Taizo Wada, Masayuki Ishine, Yasuyo Ishimoto, Mayumi Hirosaki and Yoko Sakamoto.

Footnotes

Competing interests: none.

Patient consent: Patient/guardian consent was obtained for publication.

REFERENCES

  • 1.Stout JE, Yu VE. Legionellosis. N Engl J Med 1997; 337: 682–7 [DOI] [PubMed] [Google Scholar]
  • 2.Weir AI, Bone I, Kennedy DH. Neurological involvement in legionellosis. J Neurol Neurosurg Psychiatry 1982; 45: 603–8 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Johnson JD, Raff MJ, Van Arsdall JA. Neurologic manifestations of Legionnaires’ disease. Medicine 1984; 63: 303–10 [DOI] [PubMed] [Google Scholar]
  • 4.Lees AW, Tyrrell WF. Severe cerebral disturbance in Legionnaires’ disease. Lancet 1978; 2: 1336–7 [DOI] [PubMed] [Google Scholar]
  • 5.Bamford JM, Hakin RN. Chorea after legionnaire’s disease. Br J Med 1982; 284: 1232–3 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Pendlebury WW, Perl DP, Winn WC, Jr, et al. Neuropathologic evaluation of 40 confirmed cases of Legionella pneumonia. Neurology 1983; 33: 1340–4 [DOI] [PubMed] [Google Scholar]
  • 7.Friedman HM. Legionnaires’ disease: clinical features of 24 cases. Ann Intern Med 1978; 89: 297–309 [DOI] [PubMed] [Google Scholar]
  • 8.Kennedy DH, Bone I, Weir AI. Early diagnosis of legionnaires’ disease: distinctive neurological findings. Lancet 1981; 1: 940–1 [DOI] [PubMed] [Google Scholar]
  • 9.Andersen BB, Sogaard I. Legionnaires’ disease and brain abscess. Neurology 1987; 37: 333–4 [DOI] [PubMed] [Google Scholar]
  • 10.Shelburne SA, Kielhofner MA, Tiwari PS. Cerebellar involvement in legionellosis. South Med J 2004; 97: 61–4 [DOI] [PubMed] [Google Scholar]
  • 11.Warner CL, Fayad PB, Heffner RR., Jr Legionella myositis. Neurology 1991; 41: 750–2 [DOI] [PubMed] [Google Scholar]
  • 12.Morgan JC, Cavaliere R, Juel VC. Reversible corpus callosum lesion in legionnaires’ disease. J Neurol Neurosurg Psychiatry 2004; 75: 651–4 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Kashiwagi A, Kashiwagi T, Nishikawa T, et al. Hemispatial neglect in a patient with callosal infarction. Brain 1990; 113: 1005–23 [DOI] [PubMed] [Google Scholar]

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