(2022) 22:506
Zhu et al. BMC Neurology
https://doi.org/10.1186/s12883-022-03021-5

Open Access

CASE REPORT

Cerebral infarct induced by severe
leptospirosis‑a case report and literature review
Zhongli Zhu1*†, Jian Feng1*†, Yong Dong2, Bin Jiang2, Xiong Wang3 and Fuxiang Li1*   

Abstract
Background: Although most leptospirosis is mild, the severe form can cause multiple complications, with a fatality
rate of over 50% even with ICU support. The clinical manifestations of leptospirosis vary depending on organs and
tissues involved. Both cerebral artery and coronary artery can be damaged by leptospirosis. Although cerebral arteritis
induced by leptospirosis has been reported, cerebral infarction caused by leptospirosis is rarely reported.
Case presentation: We report the case of a 79-year-old man admitted to intensive care unit (ICU) because of 3 days
duration of fever, bloody sputum and dyspnea. Five days before he was admitted to hospital, he had harvested rice in
flooded fields. After admission, leptospira interrogans DNA sequence was identified in bronchoalveolar lavage fluid
(BALF) by next-generation sequencing (NGS). Microscopic agglutination test (MAT) showed the serum antibody of
Mini serovars was 1,600 and Hebdomadis serovars was 800. On the eighth day of admission, the patient noted left
hemiplegia. Cranial CT scan revealed low-density shadow in the right basal ganglia, so cerebral infarction was diagnosed. The patient’s condition rapidly deteriorated and he died on the eleventh day of admission despite penicillin
treatment, invasive mechanical ventilation and continuous renal replacement support.
Conclusion: Neurologic leptospirosis manifested as cerebral occlusion, although rare, might be deadly and should
not be ignored.
Keywords: Case report, Leptospirosis, Cerebral infarct, Next-generation sequencing (NGS), Microscopic agglutination
test (MAT)
Background
Leptospirosis, also called Weil’s disease, is a zoonotic
infectious disease caused by pathogenic strains of the
bacterium Leptospira. Although it has a worldwide distribution, it is especially prevalent in east/south-east
Asia and South America [1]. Although most leptospirosis is mild, severe types of the disease can cause acute
respiratory distress syndrome (ARDS), acute hepatic
failure, acute kidney injury (AKI), and multiple organ
†

Zhongli Zhu and Jian Feng contributed equally to this work.

*Correspondence: lfx98@163.com
1

Department of critical care medicine, The General Hospital of Western
Theater Command, 270 Tianhui Road, Chengdu, Sichuan 610083, China
Full list of author information is available at the end of the article

dysfunction syndrome (MODS) [2]. The case-fatality
rate of severe leptospirosis can rise to 52% even with
ICU support [3]. It is estimated that annually there are
1.03 million cases and 58,900 deaths attributed to leptospirosis worldwide, with resource-poor countries having the highest morbidity and mortality, particularly
in regions where the burden of leptospirosis has been
underappreciated [4].
The clinical manifestations of leptospirosis are complicated because of the difference of impaired organs or
tissues. Generally, the clinical signs and symptoms of leptospirosis include chills, high fever, weakness, headache,
myalgia (especially gastrocnemius tenderness), superficial lymphadenectasis, and conjunctival congestion [5].
Leptospirosis has a biphasic course of illness. The first
phase corresponds to the multiplication and spread of

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the organism throughout the body, and the second phase
is characterized by the development of circulating antibodies and the detection of leptospires in the urine. In
the second phase, the clinical signs of leptospirosis are
more organ specific, which include hemoptysis/blood
sputum, dyspnea, oliguria, jaundice, and uveitis [6]. The
disease can be categorized into anicteric and icteric
forms, and the icteric form is the more severe form,
which accounts for 5-10% of patients [7]. Neuroleptospirosis, which is often manifested by aseptic meningitis,
intracerebral bleed, spinal extradural hematoma, myelopathy, myeloradiculopathy, Guillain-Barré syndrome,
neuropathies (mononeuritis, facial palsy), and myositis,
is usually unexplored and overlooked [8–10]; but to our
knowledge, cerebral infarction because of leptospirosis is
rarely reported [11]. In this report, we are able to identify an uncommon case of cerebral infarction caused by
leptospirosis.

Case presentation
On September 8, 2021, a 79-year-old man was admitted
to the respiratory medicine department with a complaint
of 3 days duration of fever, chills, bloody sputum and
dyspnea. He was a rural farmer and there was a flooding event because of a heavy rain in his hometown 7 days
before the onset. 2 days after the heavy rain, the patient
harvested the rice in the paddy field. The patient had
been well until 3 days before admission, when a moderate

Page 2 of 6

fever, chills and a cough productive of bloody sputum
developed. The patient received antibiotic treatment of
levofloxacin in a simple clinic in his hometown two days
after the onset, but got no improvement in fever. Moreover, the symptom of dyspnea was getting worse. After the
first treatment at the local clinic, the patient was hospitalized in the respiratory department of our hospital. The
patient reported no history of headache or myalgia and
denied having hypertension, diabetes, arrhythmia, coronary heart disease and tumor, which is consistent with
blood pressure, laboratory findings, electrocardiogram
(ECG, Fig. 1), cardiac ultrasound (Supplementary Fig. 1),
abdominal ultrasound (Supplementary Fig. 2), thorax-CT
(Supplementary Fig. 3A1-A3) and head CT (Fig. 2A1-A2)
during hospitalization.
After 1 day of hospitalization in the respiratory department, the patient was referred to the intensive care unit
(ICU) because of severe community acquired pneumonia with respiratory failure. On arrival at the ICU, the
patient was very sick and drowsy. The patient presented
tachycardia 135 beats per minute, body temperature
36℃, shortness of breath 35 times per minute, blood
pressure 82/47mmHg, and oxygen saturation 75% while
breathing ambient air. Jaundice was observed. Moist
rales could be heard in both lungs. The extremities
were cold, and the mottling score was 3. The superficial
lymph nodes were not palpable. There was no gastrocnemius tenderness. The remainder of the examination

Fig. 1 On September 8, 2021, electrocardiogram showed: (1) Sinus rhythm; (2) T wave anomaly

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Page 3 of 6

Fig. 2 Series head CT scan. A1-A2 scan obtained on illness days 8 showed a normal head CT. B1-B2 scan obtained on illness days 11 showed a
low-density shadow in the right basal ganglia

was normal. The arterial blood gas analysis showed the
following values: potential of hydrogen (PH) 7.44, partial
pressure of carbon dioxide (­PCO2) 24.6 mmHg, partial
pressure of oxygen ­(PO2) 37 mmHg(fraction of inspiration O2 45%), actual bicarbonate radical ­(HCO3) -16.7
mmol/L, base excess (BE) -6 mmol/L, lactic acid (Lac)
3.8 mmol/L. The initial laboratory test revealed leukocytosis with white blood cell (WBC) 19.98 × ­109/L, neutrophils accounting for 89.5%, thrombocytopenia with
72 × ­109 platelets/L, hypersensitive C-reactive protein
(hs-CRP): 199.66 mg/L, procalcitonin (PCT): 99.572 ng/
ml, serum creatinine(Scr): 150.00 umol/L, total bilirubin
(TBI): 63.60 umol/L, direct bilirubin (DBI): 43.50 umol/L,
and Alanine aminotransferase (ALT) and glutamic oxalacetic transaminase (AST) at 30.20 IU/L and 76.80
IU/L, respectively. An emergency chest high resolution
computed tomography (HRCT) scan was performed,
and the results revealed both lungs had patchy ground
glass opacity (GGO), a finding suggestive of pneumonia
(Fig. 1A1-A3).

Accordingly, the primary diagnosis was made as follows: (1) severe community acquired pneumonia, (2) septic shock, (3) acute respiratory distress syndrome, and 4)
multiple organ dysfunction syndrome. The patient received
treatment with tracheal intubation, invasive mechanical ventilation and fluid resuscitation(sodium lactate
ringer’s injection, 30ml / kg for 2 hours [12]). Intravenous
antibiotics (levofloxacin, 500 mg, q.d.; Imipenem/Cilastatin Sodium, 1,000 mg, t.i.d.) were administered empirically. The fever gradually eased and the oxygen saturation
improved. The blood and sputum cultures for bacteria
and fungi were sterile. On September 13, a head CT scan
was obtained which appeared normal (Fig. 2A1-A2) and
the second chest CT scan showed most of the pulmonary
ground glass opacity absorbed (Supplementary Fig. 3B1B3). The bedside bronchoscopy showed a little bloody
mucous sputum in the bronchi. According to the patient’s
clinical manifestation and laboratory test results, we highly
suspected he must be infected by some unknown pathogenic microorganism. On the 5th day after admission, we

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(2022) 22:506

employed next-generation sequencing technique to detect
etiology in the bronchoalveolar lavage fluid. Leptospira
interrogans deoxyribonucleic acid (DNA) sequences were
identified by next-generation sequencing analysis two days
later. Then, we sent his blood to local disease control and
prevention center to verify the next-generation sequencing results and the results of serum antibody titre tested
by microscopic agglutination test were as follows: Leptospirosis interrogans serogroup Mini serovar for 1,600 and
Leptospirosis interrogans serogroup Hebdomadis serovar
for 800. We found the patient presented with left upper and
lower limb mobility disorder on September 15, and muscle
strength was grade 0. A second head CT scan (Fig. 2B1B2) was performed on September 16th, and the results
showed cerebral atrophy and a low-density shadow in the
right basal ganglia. Compared with the first head CT scan
on September 13th (Fig. 2A1-A2), the low-density shadow
in the right basal ganglia was a new lesion. Therefore, the
final diagnosis was as follows: (1) leptospirosis, (2) septic
shock, (3) acute respiratory distress syndrome, (4) multiple organ dysfunction syndrome, and (5) Cerebral infarct.
The patient was treated with intravenous penicillin 0.4 mU,
q8h on September 16th. 7 h after the first dosage of penicillin, the patient’s condition deteriorated, with an abrupt
fever of 40℃ and oxygen saturation dropped to 82%. The
patient was considered to have developed Herxheimer
reaction and was immediately given sedatives and intravenous hydrocortisone. Thereafter, the patient experienced
a period of decreasing body temperature and increasing
oxygen saturation. Nevertheless, the patient’s condition
deteriorated further, requiring continuous pumping of norepinephrine to maintain blood pressure. Two days later, the
patient died due to sepsis-induced acute circulation failure.

Discussion and conclusions
The first human leptospirosis case in China was reported
in 1937 and leptospirosis has caused several epidemics in
China in the last century [13]. So far, more than 2.4 million cases and over 20,000 deaths due to leptospirosis
have been reported in China [13]. The incidence of leptospirosis has dramatically decreased in recent years, probably due to the lower leptospire-carrying rate in pigs [14].
Previously reported in the literature, the neurological leptospirosis often presents with meningitis and
clouded sensorium in the early phase and typical neurological manifestations that include headache, vomiting,
and meningeal irritation in the late phase [15]. Other
neurological manifestations include myeloradiculopathy,
myelopathy, Guillain-Barré syndrome like presentation,
meningoencephalitis, intracerebral bleed, cerebellar dysfunction, iridocyclitis and tremor/rigidity [16]. In 1975,
Chinese researchers from Wuhan Medical College first
reported that cerebral occlusion was due to cerebral

Page 4 of 6

arteritis in a leptospirosis endemic area in China where
the patients had a history of contact with pigs or contaminated water [16]. They conducted three autopsy cases and
found the pathological changes were basically the same
inflammatory cerebral arteritis and there were leptospiral bacteria on the cerebral artery wall in one case [16].
Another four cases of leptospirosis post mortem study
showed cerebral arteritis involving predominantly large
arteries at the base of the brain, especially the middle and
anterior cerebral arteries [17]. Furthermore, it seems leptospirosis can damage not only the cerebral artery, but
also the coronary artery [18, 19]. A review of cerebral
infarction caused by intracranial infection suggested that
a minority of leptospirosis patients may develop intracranial arterial disease [20]. In these cases, cerebral panarteritis involves the main trunks of larger arteries at the
base of the brain, and watershed and anterior circulation
infarctions may occur [21]. But as far as we know, cerebral
infarction caused by leptospirosis is rarely reported. This
is a rare leptospirosis case report, which was complicated
with cerebral infarction during the early stage of the disease. Based on previous studies and head CT scan results,
we speculate that the cerebral infarction of our patient
was likely caused by intracranial artery disease induced by
leptospirosis. Therefore, we emphasize that the possibility of cerebral infarction caused by leptospirosis should be
considered in the treatment of leptospirosis.
Diagnosis of leptospirosis depends on simple diagnostic
tests, which are often ignored because of a low index of clinical suspicion. Uncommon manifestation of leptospirosis,
especially when presented as an acute neurological manifestation, often poses a diagnostic dilemma leading to delayed
treatment and the potential for adverse clinical outcomes
[22, 23]. We made the same mistake until next-generation
sequencing was employed which detected the unknown
pathogenic microorganism in the lung. After that, the
sequences of Leptospira interrogans were identified in the
bronchoalveolar lavage fluid. next-generation sequencing
has the same principle of gene amplification as PCR. PCR,
which has been suggested to be an early diagnostic method
for leptospirosis in several literatures, can only detect known
sequences [15, 24, 25]. However, next-generation sequencing is a hypothesis-free approach that does not require prior
knowledge of sequence information and has the ability to
sequence millions of fragments simultaneously per run. A
previous case report of neuroleptospirosis suggested that
next-generation sequencing coupled with a rapid bioinformatics pipeline provided a clinically actionable diagnosis
of a specific infectious disease from an uncommon pathogen [26]. Hence, next-generation sequencing is increasingly
used in clinics for determining unknown etiologic infections in China. Beyond that, microscopic agglutination
test is the reference standard test for serological diagnosis

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(2022) 22:506

of leptospires and has high sensitivity and specificity [27].
According to the criteria made by the “Leptospirosis Reference Epidemiology Group” (LERG), a confirmed case of
leptospirosis should have an acute MAT titre of ≥ 1 in 400
or a four-fold rise of titre between acute and convalescent
samples. A probable case is defined when the MAT titre is
≥ 1 in 100 in a non-endemic area [28]. This case showed the
antibody titre detected by the microscopic agglutination test
method on the 10th day of admission as follows: Leptospirosis interrogans serogroup Mini serovar for 1,600 and Leptospirosis interrogans serogroup Hebdomadis serovar for 800.
Although there was no comparison between Mini serovar
and Hebdomadis serovar, the titre of antibody was so high
that we could draw the conclusion of leptospirosis. Notably,
the serum contained a high level antibody of two types of
leptospira serovar, both of which belong to the Leptospira
interrogans serogroup. We speculated that the patient may
in fact be simultaneously infected by two types of bacterium Leptospira since the patient lived in an area where it
is endemic and both serovars are common pathogens [29].
Therefore, the possibility that two types of bacterium leptospira had the same cross antigen could not be excluded [25].
Consequently, for severe patients with atypical symptoms
but suspected infectious disease, we recommend that eligible hospitals should perform next-generation sequencing
testing. Then, according to the results of next-generation
sequencing, the examination and treatment should be further improved. Once leptospirosis is diagnosed, mild cases
may not require antibiotics. However, appropriate therapy
with intravenous penicillin or ceftriaxone should be initiated empirically for severe disease. The role of steroids in
the treatment of leptospirosis phase is controversial [30,
31]. Based on our clinical experience, we believe that steroid hormones should be considered in the management of
critically ill patients. Furthermore, since the prognosis of
neuroleptospirosis is largely unknown, we recommend routine treatment of cerebral infarction on the basis of systemic
treatment of leptospirosis.
In conclusion, leptospirosis is a global zoonosis caused
by pathogenic strains of the bacterium Leptospira. It is
often presented with atypical clinical manifestations,
which makes diagnosis challenging. Clinicians practising
in tropical or endemic regions should consider leptospirosis infection in patients presenting with acute fever of
unknown cause. Neurologic leptospirosis manifested as
cerebral occlusion, although rare, might be deadly and
should not be ignored.
Abbreviations
ICU: intensive care unit; BALF: broncho alveolarlavage fluid; DNA:
deoxyribonucleic acid; NGS: next-generation sequencing; CT: computed
tomography; HRCT​: high resolution CT; MAT: microscopic agglutination test; ARDS: acute respiratory distress syndrome; AKI: acute kidney
injury; MODS: multi-organ dysfunction; GGO: ground glass opacities; PCT:

Page 5 of 6

procalcitonin; CRP: C-reactive protein; Scr: serum creatinine; TBI: total
bilirubin; DBI: direct bilirubin.

Supplementary Information
The online version contains supplementary material available at https://​doi.​
org/​10.​1186/​s12883-​022-​03021-5.
Additional file 1: Supplementary Fig 1. Cardiac ultrasound on September 10, 2021 showed: 1. Right heart enlargement; 2. Severe mitral
regurgitation and mild pulmonary hypertension; 3. Left ventricular systolic
function is acceptable.
Additional file 2: Supplementary Fig 2. Abdominal ultrasound on
September 10, 2021 showed: there were no abnormalities in the liver,
gallbladder, pancreas, spleen and kidney
Additional file 3: Supplementary Fig 3. Series chest high resolution CT
scans during his stay in the hospital. A1-A3 scan obtained on illness days
3 showed bilateral patchy ground-glass opacities in both lungs. B1-B3
scan obtained on illness days 8 showed most of the ground glass opacity
absorbed. C1-C3 scanobtained on illness days 11 showed apparent infiltration in both lungs, predominantly in the lower parts of lungs.
Acknowledgements
Not applicable.
Authors’ contributions
ZZ and JF analyzed the clinical data and wrote the manuscript. YD, BJ and XW
carried out the epidemiological investigation and collection of clinical data.
FL led the clinical treatment and reviewed the article. All authors read and
approved the final submission.
Funding
This work was supported by the Sichuan Province Cadre Health Research
Project (2022-1303);and the General Hospital of Western Theater Command
Military Medical Research Project of China (2019LH05).
Availability of data and materials
The datasets used and/or analyzed during the current study are available from
the corresponding author on reasonable request.

Declarations
Not applicable.Consentfor publication
Written informed consent for publication of this case report was obtained
from the patient’s son. A copy of the consent form is available for review by
the editor of this journal.
Competing interests
The authors declare that they have no competing interests.
Author details
1
Department of critical care medicine, The General Hospital of Western
Theater Command, 270 Tianhui Road, Chengdu, Sichuan 610083, China.
2
Department of critical care medicine, Dazhu County People’s Hospital, 99
Qingnian Road, Sichuan, Dazhou 635199, China. 3 Department of cardiovascular medicine, The General Hospital of Western Theater Command, 270 Tianhui
Road, Chengdu, Sichuan 610083, China.
Received: 22 March 2022 Accepted: 9 December 2022

References
1. Ricaldi JN, Swancutt MA, Matthias MA. Current trends in translational
research in leptospirosis. Curr Opin Infect Dis. 2013;26:399–403.
2. Karnik ND, Patankar AS. Leptospirosis in Intensive Care Unit. Indian J Crit
Care Med. 2021;25:134–7.

Zhu et al. BMC Neurology

3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.

31.

(2022) 22:506

Chawla V, Trivedi TH, Yeolekar ME. Epidemic of leptospirosis: an ICU experience. J Assoc Physicians India. 2004;52:619–22.
Costa F, Hagan JE, Calcagno J, et al. Global morbidity and mortality of
leptospirosis: a systematic review. PLoS Negl Trop Dis. 2015;9:e0003898.
Hu W, Lin X, Yan J. Leptospira and leptospirosis in China. Curr Opin Infect
Dis. 2014;27:432–6.
Guerra MA. Leptospirosis. J Am Vet Med Assoc. 2009;234:472–8, 430.
Wunder EA Jr, Eshghi A, Benaroudj N. Editorial: pathogenesis of Leptospira. Front Cell Infect Microbiol. 2018;8:322.
de Souza AL. Neuroleptospirosis: unexplored & overlooked. Indian J Med
Res. 2006;124:125–8.
Panicker JN, Mammachan R, Jayakumar RV. Primary neuroleptospirosis.
Postgrad Med J. 2001;77:589–90.
Bandara A, Kalaivarny G, Perera N, Indrakumar J. Aseptic meningitis as the
initial presentation of Leptospira borgpetersenii serovar Tarassovi: two
case reports and a literature review. BMC Infect Dis. 2021;21:488.
Cheng MK. A review of cerebrovascular surgery in the People’s Republic
of China. Stroke. 1982;13:249–55.
Evans L, Rhodes A, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021.
Intensive Care Med. 2021;47:1181–247.
Shi M, Jiang X. [Progress in the epidemiologic study of weil’s disease in China
in recent 50 years]. Zhonghua Liu Xing Bing Xue Za Zhi. 2000;21:228–30.
Zhang C, Wang H, Yan J. Leptospirosis prevalence in chinese populations
in the last two decades. Microbes Infect. 2012;14:317–23.
Bharti AR, Nally JE, Ricaldi JN, et al. Leptospirosis: a zoonotic disease of
global importance. Lancet Infect Dis. 2003;3:757–71.
Department of neurology and laboratory department TSAHoWMc.
Leptospirosis cerebral arteritis — 616-case clinical analysis and 3 cases of
autopsy. J Wuhan Med Coll. 1975;1:19–23.
Gong YH. Leptospiral cerebral arteritis: report of 4 autopsy cases. Acta
Acad Med Wuhan. 1984;4:44–9.
Macura T, Jarczyk R. [Weil’s disease complicated by subarachnoid hemorrhage and myocardial infarction]. Wiad Lek. 1990;43:685–7.
George P. Two uncommon manifestations of leptospirosis: Sweet’s syndrome
and central nervous system vasculitis. Asian Pac J Trop Med. 2011;4:83–4.
Carod-Artal FJ. Stroke in central nervous system infections. Ann Indian
Acad Neurol. 2008;11:64–78.
Chen Y. [A clinicopathological analysis of 12 cases of cerebrovascular leptospirosis]. Zhonghua Shen Jing Jing Shen Ke Za Zhi. 1990;23:226–8, 255.
Saeed N, Khoo CS, Remli R, et al. First reported case of Neuroleptospirosis
Complicated with Anton’s Syndrome. Front Neurol. 2018;9:966.
Bhatt M, Rastogi N, Soneja M, Biswas A. Uncommon manifestation of
leptospirosis: a diagnostic challenge. BMJ Case Rep 2018;2018.
Gasem MH, Hadi U, Alisjahbana B, et al. Leptospirosis in Indonesia:
diagnostic challenges associated with atypical clinical manifestations and
limited laboratory capacity. BMC Infect Dis. 2020;20:179.
Samrot AV, Sean TC, Bhavya KS, et al. Leptospiral infection, pathogenesis
and its Diagnosis-A review. Pathogens 2021;10.
Wilson MR, Naccache SN, Samayoa E, et al. Actionable diagnosis of neuroleptospirosis by next-generation sequencing. N Engl J Med. 2014;370:2408–17.
Cumberland P, Everard CO, Levett PN. Assessment of the efficacy of an
IgM-elisa and microscopic agglutination test (MAT) in the diagnosis of
acute leptospirosis. Am J Trop Med Hyg. 1999;61:731–4.
World Health O. Report of the second meeting of the leptospirosis burden
epidemiology reference group. Geneva: World Health Organization; 2011.
Tang Tianyong WJa. Sun Yongqing. Leptospirosis two outbreak point
characteristics of epidemiological investigation of the outbreak in Dazhu
County of Sichuan Province. j Med Pest Control. 2017;33:739–41.
Xavier V, Baby B, George JM, Ittyachen AM. Covid-19 and leptospirosis,
pulmonary involvement and response to steroids: a comparative observational study from a rural tertiary care center in Kerala. J Family Med
Prim Care. 2022;11:294–8.
Gangula RS, Prabhu MM, Stanley W. Weil syndrome causing autoimmune
haemolytic anaemia. Natl Med J India. 2019;32:88–9.

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