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editorial

Indian Pediatr 2018;55: 25-26

Scrub Typhus Meningitis Versus Acute Bacterial Meningitis and Tuberculous Meningitis

 

Stalin Viswanathan

Department of General Medicine, Indira Gandhi Medical College & Research Institute, Kathirkamam, Puducherry, India.
Email: [email protected]
 


M
eningitis in the form of cerebrospinal fluid (CSF) pleocytosis (lymphocytes predominant) in a patient with scrub typhus diagnosed by the presence of eschar and/or immunological means would constitute scrub typhus meningitis (STM). This comes under a broad umbrella of diseases causing aseptic meningitis – spirochetal, viral, rickettsial, tubercular, neoplastic, and drug-related meningitis [1]. This contrasts with acute bacterial meningitis (ABM) where neutrophils are predominant in the cerebrospinal fluid (CSF), and bacteria identified by Gram stain, culture, or immunological tests.

Kakarlapudi and colleagues [2], in this issue of Indian Pediatrics, reported a retrospective analysis of 123 children with meningitis managed in their department over a period of 5 years. They found that children with STM were older than children with either bacterial or tuberculous meningitis, and had a better prognosis than the other arms. Thrombocytopenia and splenomegaly were more often associated with STM. Information regarding hepatorenal symptoms were not available. Similarly, information about chest radiograph, liver function and renal function tests would have been more illuminating to this study.

Scrub typhus is a common cause of acute febrile illness in Asia, and complications include respiratory, neurological, hematological, myocardial and vasculitic manifestations [3]. STM is a spectrum ranging from aseptic meningitis to meningoencephalitis rather than a purely meningitic illness [4]. Diagnosis of STM is often expensive, and Weil Felix Test (WFT), the commonest test used for its diagnosis, has poor sensitivity. It is probably the easiest meningitis to treat as there is only one drug to be administered – doxycycline or chloramphenicol or azithromycin or rarely rifampicin. The morbidity and mortality of a diagnosed case of STM is generally low [4].

The comparison of STM with other meningitides as in this study is timely, especially in the Indian context [2]. As a physician, I think the following things should merit attention in the assessment of the differential diagnosis for acute to subacute febrile illness with meningeal signs. History of a mite bite is useful, but virtually never revealed. Respiratory symptoms (cough and breathlessness), abdominal symptoms (jaundice, abdominal pain, and diarrhea), and musculoskeletal manifestations (myalgia and arthralgia) should make a consideration of STM, while neurological symptoms (seizures, limb weakness, and coma) would be commoner in tuberculous meningitis (TBM). On examination, pulse and blood pressure (tachycardia and hypotension being more commonly seen in STM and ABM, while bradycardia and increased blood pressure seen more frequently in TBM-related raised intracranial pressure), tachypnea (ARDS and myocarditis in STM, pericardial and pulmonary tuberculosis in TBM), anemia (more in TBM), lymphadenopathy (both in STM and TBM), rashes (purpuric in ABM and maculopapular in STM), elevated JVP (myocarditis in STM, pericarditis in TBM), respiratory findings (seen in STM and TBM), hepatosplenomegaly (seen in STM and disseminated tuberculosis), arthritis (STM and ABM-meningococcal), cranial nerve deficits (sixth cranial nerve deficits in STM and TBM, cochlear nerve involvement in STM and ABM, multiple cranial nerve palsies in TBM), papilledema (TBM>ABM), vasculitic events (strokes in STM and TBM, myocardial infarction in STM), and shock (cardiogenic in STM and TBM, and septic in ABM) makes TBM a closer differential diagnosis to STM than ABM.

On working up such patients with acute meningitis, hemogram may show normal to a mild increase in counts in STM and TBM (ABM with blood leucocytosis and rarely leukopenia) and thrombocytopenia in STM (like viral meningoencephalitis or leptospirosis), and occasionally disseminated intravascular coagulation (ABM and STM). Deranged liver and renal functions and creatine kinase elevation are more common in STM. CSF lymphocytic pleocytosis is found in both STM and TBM. CSF protein content and hypoglycorrhachia do not help much in differentiation between the three, although TBM would have the highest protein in CSF. Gram stain and culture would be of use only in ABM and to a lesser extent in TBM, because of the time taken. Adenine deaminase (TBM), polymerase chain reaction (TBM, STM, and ABM), Cartridge Based Nucleic Acid Amplification Test (CB-NAAT for TBM) and Scrub IgM ELISA will help clinch the diagnosis, but are not routinely available in all institutions. Chest radiograph is useful for both STM and TBM. Fundus examination helps in TBM (papilledema and choroidal tubercles) and STM (papilledema). Basilar meningeal enhancement on contrast CT favors TBM [5].

Barring a few exceptions of drug resistance, one drug is sufficient for treating STM, especially if diagnosed early (unlike ABM where steroids and antibiotics, and TBM with steroids, antituberculous therapy and mannitol being necessary). Rifampicin, in even a single dose can cause clinical improvement [6]. In settings when the treating physician is unaware of STM or the facilities are inadequate to diagnose the same, the patient ends up in taking treatment for months for TBM, because of improvement with rifampicin [7]. Even though detection of serum IgM levels for scrub typhus is an affordable test, most patients and their caregivers thronging government institutions find the costs involved a deterrent, and need to be convinced about the need of such a test, which would prevent such a prolonged therapy and a label of their children having had TBM.

In conclusion, STM more closely mimics TBM in terms of clinical features, CSF findings and therapy, but differs in hematological features, hepatorenal and musculoskeletal dysfunction and neuro-imaging. ABM is like STM with its short duration of illness and can be well-differentiated with hematological, renal and liver profiles, CSF neutrophilia and culture positivity. In this age of evidence-based medicine, expensive tools such as PCR, CBNAAT, and IgM levels for scrub typhus are the need of the hour, but the availability is more of an exception rather than the rule. In localities where scrub typhus is endemic, empirical therapy could be instituted in patients with acute meningitis until a conclusive diagnosis is obtained. Multiorgan involvement should always make consideration of STM.

Funding: None; Competing interests: None stated.

References

1. Connolly KJ, Hammer SM. The acute aseptic meningitis syndrome. Infect Dis Clin North Am. 1990;4:599.

2. Kakarlapudi SR, Chacko A, Samuel P, Verghese VP, Rose W. Comparison of scrub typhus meningitis with acute bacterial meningitis and tuberculous meningitis. Indian Pediatr. 2018;55:35-7.

3. Charoensak A, Chawalparit O, Suttinont C, Niwattayakul K, Losuwanaluk K, Silpasakorn S, et al. Scrub typhus: chest radiographic and clinical findings in 130 Thai patients. J Med Assoc Thai. 2006;89:600.

4. Misra UK, Kalita J, Mani VE. Neurological manifestations of scrub typhus. J Neurol Neurosurg Psychiatry. 2015;86:761-6.

5. Marais S, Thwaites G, Schoeman JF, Török ME, Misra UK, Prasad K, et al. Tuberculous meningitis: A uniform case definition for use in clinical research. Lancet Infect Dis. 2010;10:803-12.

6. Liu Q, Panpanich R. Antibiotics for treating scrub typhus. Cochrane Database Syst Rev. 2002;3:CD002150.

7. Viswanathan S, Muthu V, Iqbal N, Remalayam B, George T. Scrub typhus meningitis in South India – a retrospective study. PLoS One 2013;8:e66595.

 

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