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\begin{document}

\title{``A Case of Acute Encephalitis Syndrome and Cranial Nerve Palsy
secondary to Scrub Typhus: A Rare Presentation from Western Nepal''.}



\author[1]{SK Lamichhane}%
\author[2]{Eliz Achhami}%
\author[2]{Satyam Mahaju}%
\author[1]{Rabin Gautam}%
\author[1]{Amrit Adhikari}%
\affil[1]{Bir Hospital}%
\affil[2]{Sukraraj Tropical and Infectious Disease Hospital}%


\vspace{-1em}



  
  \date{June 11, 2024}


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\textbf{Title Page:-}

\textbf{''A Case of Acute Encephalitis Syndrome and Cranial Nerve Palsy
secondary to Scrub Typhus: A Rare Presentation from Western Nepal''.}

SK Lamichhane\textsuperscript{1}, Eliz Achhami\textsuperscript{2},
Satyam Mahaju\textsuperscript{3}, Rabin Gautam \textsuperscript{4},
Amrit Adhikari\textsuperscript{5}

\textsuperscript{1} Bir Hospital, Kathmandu, Nepal

(email:- lamichhaneak1312@gmail.com )

\textsuperscript{2} Sukraraj Tropical \& Infectious Disease Hospital,
Kathmandu, Nepal

(email:- eliz0917@gmail.com )

\textsuperscript{3} Sukraraj Tropical \& Infectious Disease Hospital,
Kathmandu, Nepal

(email:- mahaju.satyam1@gmail.com )

\textsuperscript{4} Bir Hospital, Kathmandu, Nepal

(email:- rabingautam1@gmail.com )

\textsuperscript{5} Bir Hospital, Kathmandu, Nepal

(email:- a1amrit12@gmail.com )

*Corresponding author.

Eliz Achhami, MBBS

Sukraraj Tropical \& Infectious Disease Hospital, Kathmandu, Nepal

Mobile no. : - 977-9846710319

E-mail: eliz0917@gmail.com

\textbf{ACKNOWLEDGMENT:-}

We would like to acknowledge the patient herself and her relatives who
allowed us to share their clinical report to the global platform, so
that others will be benefitted.

\textbf{CONFLICT OF INTEREST:-}

The authors would like to declare that they have no competing interests.

\textbf{A FUNDING STATEMENT:-}

No funding was generated for this case report

\textbf{AUTHORS CONTRIBUTION:-}

\begin{enumerate}
\tightlist
\item
  SK lamichhane: involved in patient management, data collection, design
  of study, manuscript writing and revision.
\item
  Eliz Achhami : design of study, data collection, evidence collection,
  manuscript writing and revision, corresponding author.
\item
  Satyam Mahaju :- design of study, data collection, evidence
  collection, manuscript writing and revision
\item
  Rabin Gautam :- design of study, data collection, manuscript revision
\item
  Amrit Adhikari:- design of study, involved in patient management,
  manuscript revision.
\end{enumerate}

\textbf{ETHICAL APPROVAL:-}

As case reports are exempt from ethical approval in our institution, our
article which describes a case report does not require additional
permissions from the Ethics committee.

\textbf{CONSENT:-}

Full written informed consent was obtained from the patient for
publication of her case, clinical images, and radiographic images. A
copy of written consent can be made available to the editor in chief of
this journal upon request.

\textbf{DATA AVAILABILITY S TATEMENT:-}

All the data generated or analyzed during this study are included in the
manuscript.

\textbf{Introduction:-}

Scrub typhus is a zoonotic rickettsiosis caused by the bacterium
Orientia tsutsugamushi. It is transmitted by larvae of the
Leptotrombidium mites and is endemic to a region called the
tsutsugamushi triangle that extends from Southeast Asia to the Pacific
Ocean \textsuperscript{1}. Scrub typhus commonly infects farmers and
field workers \textsuperscript{1}. The central nervous system (CNS) can
often be affected in scrub typhus, with neurological manifestations
being present in approximately 20\% of cases, either in the form of
acute encephalitis, meningitis, or
meningoencephalitis\textsuperscript{2}. The clinical manifestations of
scrub typhus are variable, with the involvement of nearly every system
and organ, alone or in combination \textsuperscript{3}. Recent
epidemiological studies suggest that scrub typhus is a major cause of
central nervous system infections in endemic areas
\textsuperscript{4--6}. The neurological manifestation of scrub typhus
has become an emerging public health concern beyond current endemic
areas, as ecological changes may increase the prevalence of
arthropod-borne CNS-infected populations worldwide\textsuperscript{7}.
On the other hand, delayed treatment can lead to significant
neurological creaks and even death \textsuperscript{8}.

\textbf{Case presentation}

A 17-year-old girl living in a village in western Nepal was taken to a
tertiary hospital, Bir Hospital after being referred from another health
center with chief complaints of fever for 17 days and altered sensorium
of 4 days duration. She had a low-grade fever initially which got
controlled partially with over-the-counter medication. The fever was
insidious onset, gradually progressive but this time it was associated
with headache, vomiting, and altered sensorium. She had no history of
photophobia, ear discharge, convulsions, or focal neurological deficit.
She was then taken to a nearby hospital from where she was referred to
our hospital with a provisional diagnosis of meningitis. There was no
similar history in the past and her family history was non-significant.

When she arrived at the emergency department of Bir Hospital, her
axillary temperature was 101.2\selectlanguage{ngerman}°F, pulse was 86/min and blood pressure
was 140/100 mm Hg. The respirations were regular with a rate of 18 per
minute and oxygen saturation was 96\%. She had no eschar, rashes, or
lymphadenopathy, pupils were normally responsive. The examination of
respiratory system revealed normal vesicular sounds over both lungs
without any added sounds. The cardiovascular examination was
unremarkable.

On neurological examination, her Glasgow Coma Scale (GCS) was E3V4M6
(i.e. 13/15). She was drowsy and confused. Motor and sensory examination
revealed normal findings, superficial and deep tendon reflexes were
normal and bilateral planters were flexor. Cranial nerve examination
revealed bilateral lateral rectus palsy (Figure 1 and 2), dysphagia,
regurgitation of food on attempted feeding, dysarthria, and left sided
upper motor neuron (UMN) type facial palsy (Figure 3).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Figure 1: Left lateral rectus palsy in left gaze.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Figure 2 :Right lateral rectus palsy in right gaze.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

Figure 3: Decreased facial crease on left side.

The complete blood count revealed a total leucocyte count (TLC) of
6000/mm with 40\% neutrophils, 50\% lymphocytes, 8\% monocytes, and 2\%
eosinophils. The hemoglobin was 9.4 g/L with a mean corpuscular volume
of 79 fL and the platelet count was 320000/mcL. There was mild hepatic
dysfunction with aspartate transaminase of 63 IU/L and alanine
transaminase of 66 IU/L. Total serum bilirubin was 0.5 mg/dL and albumin
was 4 g/dL. Serum sodium, potassium, calcium, and phosphorus were within
normal limit. The renal functions were normal with urea of 16 mg/dL and
creatinine of 0.8 mg/dL.

Blood and urine cultures were sterile. Serological tests for dengue IgM
antibodies and NS1 antigen, herpes simplex and Japanese B encephalitis
IgM antibodies were negative. Simultaneous search for other tropical
infections like malaria, and leptospirosis were negative, however, Scrub
IgM was positive. A guarded lumbar puncture was performed and the CSF
analysis yielded a cell count of 16 cells \selectlanguage{greek}μ/\selectlanguage{english}L with 80\% lymphocytes and
20\% neutrophils. Total protein was elevated to 125 g/dL, glucose was 82
mg/dL and adenosine deaminase was 2.5 IU/L. No organism was seen on the
Gram stain, Ziehl-Neelsen stain, and India ink stain. CSF cultures were
sterile and PCR was negative for herpes simplex virus (HSV) and
Mycobacterium tuberculosis. The Magnetic resonance imaging (MRI) of
brain was done and MRI of brain reveled multiple mildly increased
T2DM/FLAIR signal in midbrain, pons and in left middle cerebellar
peduncle (Figures 4, 5 and 6).

Ceftriaxone, which was already started at the center where she was
referred, was continued and the dose was doubled to 2gm two times per
day. Acyclovir was added intravenously at a dose of 500 mg times per day
and was discontinued after exclusion of herpes simplex encephalitis.
Dexamethasone was started at a high dose (1gm) to ease cerebral edema.
Ceftriaxone was substituted with doxycycline 100 mg two times per day
intravenously after scrub typhus was diagnosed. Two days later, the
fever subsided, and gradually she was able to communicate verbally and
eat on her own. Objective improvement was documented on MRI. Doxycycline
was administered for a total of 2 weeks.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

Figure 4. Hyperintense T2/FLAIR Axial images on left insular lobe and
adjacent thalamus.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

Figure 5. Hyperintense T2/FLAIR coronal images on left insular lobe and
adjacent thalamus.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}

Figure 6: Hyperintense T2 Axial images with mildly incresed signal in
pons.

\textbf{Discussion:-}

There have been few attempts to study scrub typhus in Nepal. In 1981, a
high probability of scrub typhus was identified in Nepal by detecting
high antibody titers (10\%) in healthy adults. IgM antibodies to O.
tsutsugamushi were positive in samples from various regions, including
30 districts in Nepal. Positive cases have been found in different
ecological regions of Nepal \textsuperscript{9}.

Humans are infected by the bite of the larvae of the leptothrombidium
mite. From the bite site, bacteria are distributed throughout the body
via blood and lymph. It induces endothelial injury, leukocyte
perivascular infiltration, increased vascular permeability, and an
vasculitic response with severe microvascular thrombosis leading to
organ damage \textsuperscript{1,10}. Classically, scrub typhus presents
with fever, headache, cough, myalgia, arthralgia, lymphadenopathy, and
maculopapular rash that begins from the trunk and spreads to the
limbs\textsuperscript{11--13}. The 'eschar', which are thought to be the
hallmark of the disease, are the bites of these chiggers that creates
wound similar to 'cigarette burns' \textsuperscript{1,10}.
''Characteristic'' symptoms of scrub typhus have been occasionally
reported, with the characteristic crust occurring in only 20\% of
patients and lymphadenopathy in 24\%. Nevertheless, the eschar occurs
more frequently in adults, and conversely, and conversely organanomegaly
can occur in children. However, the absence of these signs should not
rule out scrub typhus infection, as these features are present in only 1
in 4-5 patients with confirmed CNS scrub typhus. Given its potential
impact on long-term morbidity, clinicians should be alert to the
possibility of acute convulsive activity in children with central
nervous system scrub typhus \textsuperscript{14}. The microbe has an
increased propensity of infecting organs that are highly vascularized,
like the liver, brain, heart, and lungs \textsuperscript{11}. Hence,
beginning from 2nd week, the infection, if untreated, progresses to
complications like acute diffuse encephalomyelitis, encephalopathy,
meningitis, cranial nerve palsies, congestive heart failure, vasculitis,
myocarditis, pneumonia, acute respiratory distress syndrome, acute renal
failure, gastrointestinal bleeding, alterations in liver functions and
pancreatitis \textsuperscript{11--13,15}. Among the complications,
myocarditis and encephalitis are the most life-threatening
ones\textsuperscript{16}. Doxycycline is the drug of choice and
azithromycin is the drug of choice for children and pregnant
women\textsuperscript{17}.

Despite the growing number of clinical studies addressing the
neurological complications of tsutsugamushi disease, there are
surprisingly few studies to clarify the underlying mechanisms of
neuroinvasion and neuroinflammation \textsuperscript{8}. Spread of
bacteria from the periphery to the central nervous system occurs by
hematogenous spread \textsuperscript{18,19}.

Although the exact mechanism of entry into the central nervous system is
unknown, there is evidence that direct entry may occur through damage to
the microvascular endothelium or disruption of the blood-brain barrier
through transcellular translocation of bacteria, which can occur
independently or by way of macrophages that have engulfed the bacterium.
After entering the central nervous system, it activates specific
transcription factors, such as the nuclear factor kappa B, which causes
inflammation {[}14{]}. Orientia tsutsugamushi has an endothelial cell
tropism and invades dendritic cells, monocytes and tissue macrophages.
Endothelial invasion causes vascular injury with intestinal perivascular
mononuclear infiltration leading to complications \textsuperscript{20}.

Several neurological syndromes have been reported in association with
scrub typhus. Literature review reveals case reports of acute transverse
myelitis, myoclonus, parkinsonism, and acute disseminated
encephalomyelitis \textsuperscript{21--23}. Solitary or multiple cranial
neuropathy is a well-known neurological manifestation of scrub typhus
infection \textsuperscript{2}. Cranial nerve disorders such as facial
paralysis, sensorineural hearing loss, trigeminal neuralgia, and
diplopia due to abduction paralysis were
observed\textsuperscript{24--27}. Few authors suggest that scrub typhus
should be considered as a differential diagnosis in all patients with
aseptic meningitis with renal or hepatic impairment living in endemic
areas\textsuperscript{28}. They found that the CSF profile mimics
tuberculous meningitis or viral meningitis. CSF had predominantly
lymphocytic pleocytosis, elevated protein with low or normal glucose.

As per the definition, acute encephalitis syndrome presents with the
fever in association with seizure, altered mental status and the focal
neurological signs like ataxia, aphasia, cranial nerve palsy or
hemiparesis \textsuperscript{12}. Our patient presented with the
symptoms of fever, headache, vomiting, and altered mental status
associated with the signs of bilateral lateral rectus palsy, dysphagia,
regurgitation of food, dysarthria, and left-sided UMN type facial palsy
that is suggestive of acute encephalitis syndrome with cranial nerve
palsy.

The Neuroimaging findings for meningoencephalitis due to scrub typhus
are quite limited. There have been reports of radio imaging findings of
lesions on a white matter involving the subcortical, periventricular
deep white matter, corpus callosum, cerebellar peduncles, brain stem,
and basal ganglia, as well as grey matter lesion and
microhemorrhages\textsuperscript{29}. Kar et. al(2014) have reported the
presence of diffuse cerebral edema along with T2-weighted and FLAIR
hyperintensities in the putamen and thalamus, suggesting brain
parenchymal involvement\textsuperscript{12}. The diagnosis of
encephalitis in our case was further supported by the multiple mildly
increased T2DM/FLAIR signal in the midbrain, pons, and left middle
cerebellar peduncle.

\textbf{Conclusion:-}

In conclusion, we report a case of scrub typhus presenting as acute
encephalitis and cranial nerve palsy treated successfully with high-dose
dexamethasone and doxycycline. The unique feature in our case was the
unusual involvement of cranial nerves due to scrub typhus. Therefore,
while evaluating a case of AES with cranial nerve palsy with suspected
infectious disease etiology, it is essential to consider scrub typhus
among differential diagnoses, especially in the region of the
tsutsugamushi triangle. A timely diagnosis and treatment can help
prevent the development of various complications and can help with
earlier recovery of patients.

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doi:10.1177/19418744211016107\selectlanguage{english}
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