INTRODUCTION
Fusarium species are important plant pathogens that occasionally cause infection in humans.
Fusarium species can cause superficial infections (superficial keratitis, onychomycosis, allergic
sinusitis) in immunocompetent individuals.[1] However, infection in the immunocompromised population is typically invasive and
disseminated.[1]
[2] We report a case of concomitant Fusarium meningitis in a patient with tubercular meningitis (TBM).
CASE REPORT
A 14-year-old 34 kg girl presented to us with the complaints of a prolonged febrile
illness and 1 day history of repeated generalised tonic-clonic seizures (GTCS). The
patient had a history of low-grade fever (without chills and rigors) for 9 months
and 4 months ago, following a persistent headache she was diagnosed to have TBM on
the basis of cerebrospinal fluid (CSF) examination. The patient was receiving standard
doses of isoniazid, rifampin, pyrazinamide and pyridoxine for the past 4 months. There
was no history of trauma, previous seizures, skin lesions or family history of tuberculosis
or hypertension. About 15 days before hospitalisation, she had a persistent severe
headache for which analgesics and tablet dexamethasone (4 mg thrice a day) was started.
After that, her headache decreased in severity but 7 days before admission the severity
of a headache again increased. Before presenting to us, she also had repeated GTCS
since 1 day. On presentation, her blood pressure was 150/108 mmHg and her other systemic
examination was within normal limits. The patient was managed symptomatically with
antiepileptic medications.
Apart from haemoglobin level of 10.4 g/dl and white blood cell count of 18,390 cells/mm3 (63% neutrophils and 30% lymphocytes), her other haematological investigations and
non-contrast computed tomography scan of the head were normal. The serological markers
for hepatitis and HIV were non-reactive. On the basis of clinical presentation and
available test reports, CSF examination was done, and no further ophthalmological
examination or tests for detection of haematological malignancy or brain abscess were
attempted.
The CSF examination of the patient revealed total leucocyte count, protein and sugar
levels to be 306 cells/mm3 (lymphocytes 60% and neutrophills 40%), 210 mg/dl and 106 mg/dl, respectively. On
direct microscopy of CSF, hyaline, narrow, septate and branching fungal hyphae were
seen. The sample was inoculated onto Sabouraud’s Dextrose agar with and without cycloheximide
and was incubated both at 25°C and 37°C. The cultures yielded colonies that were cottony
white to pink with a floccose aerial mycelium. The lactophenol cotton blue mount was
prepared which when examined under ×10 followed by ×40 objective of the microscope
revealed, one-/two-celled, oval microconidia, 8–9 mm × 2–3 mm in size, grouped in
chains and produced from simple lateral phialides [Figure 1]. The organism was identified to be Fusarium spp. The blood culture did not yield any fungus, but the repeat CSF examination (before
starting antifungal therapy) again revealed Fusarium spp. The patient was treated with amphotericin B (intravenous) (loading dose of 0.75
mg/kg followed by 1 mg/kg)[3] for 14 days along with the on-going antitubercular medications. The patient improved
and the CSF examination following 14 days of antifungal therapy yielded no fungal
growth. The patient was discharged subsequently after 25 days of hospital admission
with on-going antitubercular and antiepileptic medications.
Figure 1: Lactophenol cotton blue mount showing macro and micro conidia of Fusarium
DISCUSSION
The different fungi implicated in causing meningitis are Cryptococcus neoformans, Coccidioides immitis, Candida sp., Histoplasma capsulatum, Aspergillus sp., Sporothrix schenckii, and Blastomyces dermatitidis.[4] The most common route of entry of fungi to the human body is through inhalation
of airborne fungal spores. The initial pulmonary infection may be asymptomatic and
is often self-limited. However, a dormant localised pulmonary fungal infection can
remain, and an immunocompromised status may allow the fungus to reactivate and disseminate
to the central nervous system (CNS). Organ transplant recipients, patients on chemotherapy,
patients with immunocompromised state or haematological malignancies have increased
the risk for fungal infection of CNS.
The skin and respiratory tract are the primary portals of entry of Fusarium species into the human body. In humans, Fusarium species cause superficial, locally invasive and disseminated infections. The clinical
form of fusariosis depends largely on the immune status of the host, and the severe
form of infection is usually encountered in immune compromised patients.[1] Fusarium brain abscess and meningitis has been reported in a patient with chronic infectious
mononucleousis syndrome and immunodeficiency where the patient died despite abscess
aspiration and treatment with amphotericin B.[2] However, another patient of the chronic granulomatous disease had long standing
chronic disseminated Fusarium infection with multiple soft tissue abscesses and was successfully treated with antibiotic
and antifungal therapy.[5] However, Fusarium infection in a patient with TBM has rarely been reported. Fusarium is highly resistant to conventional antifungal drugs and amphotericin B and voriconazole
are the two antifungal agents that are used with some success to treat Fusarium infection in human.
In our case, the patient had TBM with concomitant Fusarium meningitis causing persistence of meningitis in spite of anti-tubercular therapy.
She probably had a state of compromised immune status due to on-going steroid therapy
and poor nutritional status which lead to the Fusarium infection. CNS vascular invasion by Fusarium has been noted before other organ system involvement in disseminated Fusarium infection.[2] This might explain the CNS invasion by Fusarium in our patient. In this report, we want to emphasise the fact that due to on-going
steroid therapy, patients of TBM can have a compromised immune status, leading to
opportunistic fungal infection.
Fungal infection of CNS many a times becomes a diagnostic and therapeutic challenge.
In patients with TBM, that is unresponsive to anti-tubercular therapy a thorough microbiological
evaluation, might detect an unlikely fungal pathogen leading to initiation of timely
management.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
