Download Opportunistic Central Nervous System Infections

Opportunistic Central Nervous
System Infections
John H. Samies, MD, FSHEA, CWS
Infectious Diseases / Internal Medicine
January 31, 2012
Overview
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Define opportunistic infectious agents of the CNS
Define high risk circumstances & populations
Discuss pathogenesis of infectious agents
Illustrate diagnostic approach & differential determination
Describe some associated management issues
Variety of organisms cause CNS infection
This is all about
• THE LOCATION
• THE HOST
• THE SETTING
Location , location, location
By Location
– Meningitis: Inflammation of the meninges-the
surrounding 3-layered membranes of the brain
and spinal cord, and cerebrospinal fluid (CSF).
– Encephalitis: Inflammation of the brain itself.
– Myelitis: Spinal cord inflammation.
– Abscess: Accumulation of infectious material
and microorganisms within the CNS.
Meningitis
ENCEPHALITIS
MYELITIS
ABSCESS
The host
The Host
• Opportunistic implies a loss of normal defense
• An intact defense system is a complex interplay
of protecting surfaces, cells and soluble factors.
• The resident flora does not normally alert the
immune system or cause disease
– In fact may be protective
• Ex : Meningococcus ( Neisseria meningitidis )
Risk factors for meningitis include :
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Age >60 years or < 5 years
Diabetes mellitus, renal or adrenal
insufficiency, hypoparathyroidism, or
cystic fibrosis
Immunosuppressive meds
Human immunodeficiency virus
Crowding (eg, military recruits and
college dorm residents),
Splenectomy (either surgical or due to
splenic disease such as infarction ) and
sickle cell anemia , which increase the
risk of meningitis secondary to
encapsulated organisms
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Alcoholism and cirrhosis
Recent exposure to patients with
meningitis,
Contiguous infection (eg, sinusitis or
mastoiditis)
Dural defect (eg, traumatic, surgical,
congenital)
Thalassemia major
Injecting (IV) drug use
Bacterial endocarditis
Ventriculoperitoneal shunt
Malignancy (increased risk of Listeria
species infection)
Some cranial congenital deformities
Loss of defense
• Related to sheer number of pathogens
• Related to breakdown of normal host
– Alteration of resident flora
– Alteration of integumentary protection
• Skin / mucosa
– Cellular dysfunction
• Granulocyte
• Lymphocyte
• Monocyte/ macrophage
– Humoral immune dysfunction
B-lymphocyte dysfunction
• Patients with disorders that decrease Blymphocyte function are particularly
susceptible to meningitis caused by
encapsulated bacterial pathogens.
(Pneumococcus , Meningococcus )
• The presentation of bacterial meningitis is
essentially the same in normal and
compromised hosts with impaired Blymphocyte immunity.
T-lymphocyte & macrophage dysfunction
• Compromised hosts with impaired T-lymphocyte
or macrophage function are prone to develop
CNS infections caused by intracellular
pathogens.
• The most common intracellular pathogens are
the fungi, particularly Aspergillus, other bacteria
(e.g., Nocardia), viruses (i.e., HSV, JC, CMV,
HHV-6), and parasites (e.g., T. gondii).
T-lymphocyte defects
• Patients with T-lymphocyte defects
presenting with meningitis generally have
meningitis caused by Cryptococcus or
Listeria rather than toxoplasmosis or CMV
infection.
• The presence of extra-CNS sites of infection
also may be helpful in diagnosis.
• Ex: A patient with impaired cellular immunity
with mass lesions in the lungs and brain that
have appeared subacutely or chronically
should suggest Nocardia or Aspergillus rather
than cryptococcosis or toxoplasmosis.
Presentation is key clinically
• Most patients with CNS infections may be
grouped into those with meningeal signs,
or those with mass lesions.
• Most pathogens have a predictable
clinical presentation that differs from that
of the normal host.
The Setting
Settings – HIV
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HIV related CNS opportunistic infections
– Nervous system opportunistic infections are seen in about 20% of AIDS cases and
account for over 40% of AIDS related neurological manifestations.
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In HIV there is a complex interplay of immune deficits but mainly T-cell
immunity is impaired
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CNS cytomegalovirus (encephalitis )
CNS cryptococcal infection (usually meningistis)
Toxoplamosis (usually abscess)
HIV encephalitis  actually involves HIV cells in CNS
Less common : progressive multifocal leukoencephalopathy, herpes simplex and
zoster infections and tuberculosis.
HIV and Cryptococcus
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Cryptococcal meningitis is the most frequent fungal disease; a high degree
of clinical suspicion is required in patients with fever, malaise, headache or
seizures.
CSF cultures are nearly always positive
Both serum and CSF cryptococcal antigen tests are highly sensitive and
specific.
Treatment with amphotericin B and flucytosine is successful in at least
70% of first episodes but side-effects are common.
Without maintenance therapy 50% of patients relapse; fluconazole is
recommended.
HIV and CNS toxoplamosis
• Cerebral toxoplasmosis can present with focal cerebral or spinal
cord signs but also as a diffuse encephalopathy
• Negative T. gondii serology is unusual but positive serum titers
are usually not helpful.
• Treatment with sulfadiazine, pyrimethamine and folinic acid
achieves good results in 90% of the first episodes, (side-effects
common).
• Appearances on CT scan or MRI may take several weeks to
improve.
Neurosyphilis and HIV
• HIV disease appears to increase the
likelihood of neurosyphilis, and the risk of
relapse after conventional penicillin doses
• At least 3-4 weeks of appropriate therapy
are recommended.
Aspergillus
• Aspergillus infections present either as
mass lesions (e.g., brain abscess), or as
cerebral infarcts, but rarely as meningitis.
Transplants
• Infection of the CNS occurs in 5% to 10% of
transplant patients and most often manifests
as brain abscess, encephalitis, or meningitis.
• Aspergillus fumigatus, Listeria
monocytogenes, and Cryptococcus
neoformans are the most common causes of
CNS infections in post-transplant patients.
Transplantation
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Susceptibility to CNS infection after transplantation changes over time.
During the first month, CNS infection is most often caused by common
bacterial pathogens or opportunistic pathogens present in either the
transplant environment (e.g., Aspergillus species), or host (e.g.,
Mycobacterium tuberculosis).
At 1 to 6 months, immunosuppression is at its highest, resulting in
increased susceptibility to CNS infection by the herpesviruses, especially
CMV and Epstein-Barr virus (EBV), fungi, and atypical bacteria.
After 6 months, reduction of immunosuppression is accompanied by
decreased susceptibility to CNS infection. Most cases of PML and
cryptococcal meningitis occur 6 months post-transplantation.
Specific pathogens – actors
Viruses
Cytomegalovirus - CMV
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Between 50% and 80% of adults in the United States are infected with CMV
by 40 years of age
CMV is the most common virus transmitted to fetus
Approximately 1 in 150 children is born with congenital CMV
Approximately 1 in 750 children is born with or develops permanent
disabilities due to CMV
CMV
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Transmission of CMV occurs from person to person, through close contact
with body fluids (urine, saliva, breast milk, blood, tears, semen, and vaginal
fluids),
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the chance of getting CMV infection from casual contact is very small.
In the United States, about 1%-4% of uninfected mothers have primary
CMV infection during a pregnancy.
1/3 of women with primary CMV during pregnancy transmit to their fetus
NO approved treatments for pregnant women whose fetuses might be
infected with CMV.
CMV
• Cytomegalovirus –commonly infects neurons, glia, ependyma
• Often very hard to define infection versus disease in
immunocompromised hosts
• CMV disease requires clinical signs and symptoms, such as
fever, leukopenia, or organ involvement (including hepatitis,
pneumonitis, pancreatitis, colitis, meningoencephalitis, and rarely
myocarditis)
• “viral load “
JC
• Probable cause of most cases of progressive
multifocal leukoencephalopathy
• Targets myelinating oligodendrocytes
• An opportunistic infection in HIV patients
causing dementia like process
• Diagnosed by spinal fluid PCR
HH6- Human Herpes 6
• B – cell lymphotrophic virus that is the cause
of roseola – and a frequent cause of febrile
seizures
• Reactivation occurs in immune compromised
adults with HIV and lymphoma and has a
possible role in multiple sclerosis and
progressive multifocal leukoencephalopathy.
Herpes simplex
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HSV-1 infection in the immunocompromised host causes more morbidity and mortality than
in the general population
62 percent of fatalities following renal transplantation were caused by viruses, with HSV
contributing in 60 percent
In a cohort of bone marrow transplant recipients, 82 percent of seropositive patients
developed reactivation of HSV after transplantation
The prevalence of HSV-1 cutaneous infections in HIV-infected patients is in the range of 5
to 20 percent . Lesions tend to be more severe than in immunocompetent hosts, with local
destruction and persistent shedding of virus.
Toll-like receptors are important in the innate immune response. TLRs
may prevent spread of HSV from the epithelium to the brain via cranial
nerves through generation of interferons. Two known mutations in TLRs
predispose children to HSV encephalitis
Fungi
Fungal CNS infections
• With the exception of Candida albicans ( normal
flora of mucosa) most fungi get into the body
through the airway or breaks in the skin
• Invasion of the CNS with fungi can cause acute
or chronic meningitis, encephalitis, abscess or
granuloma, stroke, or myelopathy .
• A variety of fungi lead to CNS infection
Diffuse--- meningitis mainly
Coccidiodomycosis
Cryptococcosis
Candidiasis
Focal--- filamentous fungi cause granuloma or brain abscess more
often than meningitis
Aspergillosis
Mucormycosis
• Acute (sometimes called neutrophilic meningitis) has been most
frequently seen in Candida meningitis
• Cryptococcus neoformans typically causes the chronic
lymphocytic meningitis
• Coccidioides immitis causes granulomatous meningitis.
Cryptococcal CNS disease
• The majority of cryptococcoses begin as a
primary pulmonary infection.
• 5-10% of HIV + hosts develop cryptococcal
meningitis as an AIDS associated disease
• 40% of cases = first manifestation HIV
Candida CNS disease
• Candida species = normal flora of the mucous membranes and
skin.
• C albicans= the most frequent cause of meningitis and brain
abscess among Candida species.
• Less common pathogens species are C. tropicalis, C
parapsilosis, C lusitaniae, C glabrata and C krusei.
• Candida meningitis is more common in infants/ neonates than in
older patients.
CNS Candida
• In newborns, candidiasis of CNS is an infection of the
compromised or premature child.
• Candida meningitis associated with neurosurgery
• Long term antibiotics, steroids, immunosuppressive and
chemotherapeutic agents, neutropenia and AIDS promote
hematogenous dissemination
CNS Candida
• Up to 64 percent of neonates dying with invasive candidiasis
have CNS involvement
• More than 2/3 of these babies have positive CSF cultures at
some point during their disease.
Candida –scattered brain abscesses
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Multiple disseminated micro-abscesses with little or no meningeal
involvement have been consistently found in between 18 to 52% of patients
dying with invasive candidiasis.
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Very few cases of primary Candida brain abscesses have been reported in
the literature. Most have been secondary to a primary source of candidiasis,
including previous untreated episodes of candidemia.
Aspergilllus
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Aspergillus is ubiquitous saprophyte organism in soil, water and decaying vegetation. – a
filamentous fungus
Enters the body through the respiratory tract and paranasal sinuses .The invasion to CNS
follows a contiguous focus infection anatomically near to the brain or by the hematogenous
seeding.
In addition to primary infection of lungs, hematogenous dissemination is also initiated by
invasion into bloodstream via the middle ear, paranasal sinuses, eye, and mastoid or as a
result of open-heart operation
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Prolonged neutropenia and use of high-dose of corticosteroids are the main predisposing
factors in patients with solid organ transplant and cancers
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Abscesses of brain are common in disseminated aspergillosis
Aspergillus
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The genus Aspergillus includes over 185 species. Around 20 species have so far been reported
as causative agents of opportunistic infections in man.
Aspergillus niger is responsible for the black color you see in weathered wood and is a common
fungus found in splinters.
Immune suppression is the major factor predisposing to development of opportunistic infections
with Aspergillus
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It is the second most commonly recovered fungus in opportunistic mycoses following Candida
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Almost any organ or system in the human body may be involved including cerebral aspergillosis
and meningitis.
Aspergillus…..we make our own food
Disseminated infections can be seen in immunocompromised hosts.
Aspergillus produces aggressive infection by invading a cerebral vessel
producing hemorrhage and thrombosis.
Zygomycetes
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CNS zygomycosis is a fungal infection caused by class Zygomycetes such as the Genera
Rhizopus, Rhizomucor, Absidia, Mucor, Cunninghamella
opportunistic fungal infection
distribution of its different clinical types is more according to predisposing factors than on
gender, race, age or geography.
Zygomycetes thrive in a highly acid condition that has rich carbohydrate.
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diabetic ketoacidosis patient @ risk of defective phagocyte function and offers an environment
for quick invasion
Zygomycetes proliferate in neutropenic patients whose
serum
iron concentration is increased by deferoxamine
Mucormycosis- (a Zygomycete)
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Mucor spp. - filamentous fungi found in soil, plants, decaying fruits and vegetables. As well as
being ubiquitous in nature and a common laboratory contaminant, Mucor spp. may cause
infections in man, frogs, amphibians, cattle, and swine.
Mucormycosis is associated with the acidotic diabetics, malnourished children, and severely
burned patients.
Also seen in patients with leukemia, lymphoma, AIDS, and those on immunosuppressive
therapy with corticosteroids.
The infection typically involves the rhino-facial-cranial area, lungs, gastrointestinal tract, skin, or
less commonly other organ systems.
The fungi show a predilection for vessel (arterial) invasion resulting in embolization and
necrosis of surrounding tissue. The organism creates its own nutritional source.
Rhinocerebral disease in acidotic patients usually results in death, often within a few days.
Rhinocerebral Mucormycosis
Dimorphic fungi
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Among dimorphic fungi C. immitis and
Histoplasma capulatum are the frequent
organisms causing infections of the CNS.
Coccidiodes immitis
– A frequent cause of meningitis
– geographically limited to Southwest
United States and South America
countries .
– Coccidial meningitis happens in 3050% of patients with disseminated
infection.
– Can occur in an immunocomponent
human.
– Patients with HIV positive, solid
organ transplant, treated by steroids
and pregnancy are at a high risk of
dissemination
Coccidiomycosis
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Endemic in southwest United States most cases are sub-clinical.
Most common in males and agricultural workers. It is primarily a
disease of the healthy and disseminates from a primary pulmonary
site with about 30 - 50% risk of CNS involvement.
Focal symptoms are uncommon, chronic meningitis is common.
CNS Coccidiomycosis
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Although coccidioidomycosis usually occurs in otherwise healthy
immunocompetent hosts, it may also develop in
immunocompromised patients( AIDS and organ transplant
recipients).
This is especially true when coccidioidomycosis is in the CNS.
Histoplamosis
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Histoplasmosis caused by H. capsulatum is endemic in the United States,
South America, Southeast Asia and Africa .
At risk populations
– AIDS patients CNS
– patients who have solid organ transplantation
– patients treated with steroids.
Histoplasmosis
• Inhalation route – found in soil contaminated
with bird droppings
• Common in HIV-AIDS
• Initial phase is flulike illness with fever and myalgias
and cough
• Chronic phase with dissemination
• Mediastinitis commonly fatal and refractory to
treatment
Bob Dylan – ‘The answer is blowin
in the wind”
Histoplasmosis
• Central nervous system involvement occurs in 5 to 20 percent of
cases of disseminated histoplasmosis and is more common in
those with underlying immunosuppressive disorders
• Clinical presentations include (in immunocompromised):
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Meningitis plus other symptoms of disseminated histoplasmosis
Isolated chronic meningitis
Focal brain lesions
Encephalitis
Localized involvement of the spinal cord
Cryptococcus neoformans
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Cryptococcus neoformans is the causative agent of Cryptococcosis. Given the neurotropic
nature of the fungus, the most common clinical form of cryptococcosis is
meningoencephalitis.
The most commonly encountered predisposing factor =AIDS
Less common, organ transplant recipients or cancer patients receiving chemotherapeutics
or long-term corticosteroid treatment.
Cryptococcosis may also involve the skin, lungs, prostate gland, urinary tract, eyes,
myocardium, bones, and joints
The course of the infection is usually subacute or chronic.
Cryptococcus
• Globose to ovoid yeast cells that have a
capsule
• Do not produce well-developed
pseudohyphae nor true hyphae.
• Candida forms well-developed
pseudohyphae.
Parasites
Toxoplasmosis
Arthur Ashe
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Toxoplasmosis is the leading cause of focal central nervous system (CNS)
disease in AIDS. CNS toxoplasmosis in HIV-infected patients is usually a
complication of the late phase of the disease.
Typically, lesions are found in the brain and their effects dominate the
clinical presentation. Rarely, intraspinal lesions need to be considered in the
differential diagnosis of myelopathy
Toxoplasmosis
• CNS toxoplasmosis results from infection by
the intracellular parasite Toxoplasma gondii.
• Almost always due to reactivation of old CNS
lesions or to hematogenous spread of a
previously acquired infection.
• Rarely, it results from primary infection
Toxoplasmosis
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CNS toxoplasmosis begins with constitutional symptoms and headache.
Later, confusion and drowsiness, seizures, focal weakness, and language
disturbance develop. Without treatment, patients progress to coma in days
to weeks.
On physical examination, personality and mental status changes may be
observed. Seizures, hemiparesis, hemianopsia, aphasia, ataxia, and cranial
nerve palsies may be evident.
Occasionally, symptoms and signs of a radiculomyelopathy predominate.
Toxoplasmosis
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Cerebral toxoplasmosis is typically a disease of the immunocompromised.
There is an acute onset of focal neurological deficit over a few days.
The deficits are usually hemispherical (hemiparesis, apraxia, visual field defect etc)
but may less commonly present with brainstem or cerebellar signs.
There is commonly clouding of consciousness with fever and constitutional
symptoms.
Imaging shows well defined, ring enhancing, lesions with
surrounding edema. Lesions are most commonly found
in the cortex and grey matter of the diencephalon.
Toxoplasmosis
Naegleria
Pathogen: Naegleria fowleri
Route of entry: Contaminated water, through cribriform
plate
Age: Children, young adults
The Case
A 9-year-old boy was admitted to a hospital in Este, a
small town in the Veneto region (northern Italy), with a
1-day history of fever and persistent headache on the right
side. The child swam and played in a small swimming hole
associated with the Po River in northern Italy 10 days
before the onset of symptoms. At the time, the region was
experiencing an unusually hot summer.
Naegleria
• A retrograde neuronal (ie, olfactory and
peripheral nerves) pathway
Naegleria fowleri
• Infection believed to be introduced through nasal cavity and
olfactory neuroepithelium
• Symptoms include headache, lethargy, disorientation, coma
• Usually summer or fall (when we get in water)
• Rapid clinical course, death in 2-7 days after onset of symptoms
• Trophozoites can be detected in spinal fluid, but diagnosis is
usually at autopsy….PCR
• 4 known survivors treated with Amphotericin B
Acanthamoeba
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Pathogen: Acanthamoeba castellanii
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Route of entry: Probably sinus, skin lesion, eye
Anatomic Sites: Anywhere in the brain can be involved but the cerebellum,
brain stem, thalamus and anterior parts of the cerebrum are most severely
affected; the spinal cord is usually spared.
Acanthamoeba
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May or may not have history of swimming or exposure to contaminated water;
Presents as a subacute or chronic meningoencephalitis;
Symptoms include headache, fever, mental abnormalities, hemiparesis and seizures;
Patients may be immunocompromised or have HIV infection, or having some chronic
disease such as diabetes.
Trophozoites: 15-45 mm in diameter, nucleus with a dense central nucleolus, cytoplasm
contains granules and vacuoles
Trophozoites be found in the vessel wall and in areas free of inflammatory cell infiltration.
Cystic forms: in the tissue (15-20 mm in diameter) characterized by wrinkled double wall
around a stellate endocyst
Bacteria
Nocardia • Nocardia asteroides is a filamentous aerobic gram positive
bacterium that generally enters the body through the respiratory
system.
• Initial symptoms are that of pulmonary infection with cough, fever
and sputum production
• Dissemination involving the organ with brain abscess and
subcutaneous nodules being the most frequent. This is seen
exclusively in immunocompromised patients
• Delay of diagnosis = poor outcome.
“Hole
in the lung/ hole in the brain “
Not really opportunists per se
Echinococcus
Echinococcus
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Echinococcosis in humans is also called hydatid cyst disease
Hydatid disease caused by Echinococcus granulosis is primarily found in
Alaska, California, and the South-West
E. multilocularis more common in the North-Central
Dogs and wolves are definitive hosts of E. granulosis
Dogs and foxes are definitive hosts of E. multilocularis.
Dogs become infected with E. granulosis by ingesting sheep or goat
intermediate host viscera containing infective hydatid cysts; E. multilocularis
involves rodent intermediate hosts.
Transmission to humans takes place by accidental ingestion of ova of
Echinococcus shed in feces of infected dogs.
Echinococcus
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Humans become infected with E. granulosis when they accidentally ingest eggs in
contaminated foods, on vegetables or on blades of grass.
Although uncommon, this disease is potentially fatal and is on the increase.
Cerebral echinococcosis should be kept in mind in the differential diagnosis of cerebral
cystic lesions, especially in the endemic areas, where hydatid disease is a common
problem.
Hydatid cysts may mimic brain tumors so a preoperative diagnosis is important
especially in endemic areas.
Intracranial hydatid cysts should always be surgically removed without rupture. Proper
preoperative diagnosis is critical for the successful outcome of surgery. The outcome
remains excellent for unruptured cysts.
Malaria as an opportunist
(Mal =bad / Aria= air)
• HIV increases the risk of malaria infection
and the development of clinical malaria.
Conversely, malaria increases HIV
replication.
• Pregnant women transiently lose some of
their acquired immunity due to the relative
immunosuppression of pregnancy
Malaria
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Cerebral malaria (CM) involves the clinical manifestations of Plasmodium falciparum malaria
that induce changes in mental status and coma.
It is an acute, widespread disease of the brain which is accompanied by fever. The mortality
ratio is between 25-50%. Untreated, CM is fatal in 24-72 hours.
The histopathological hallmark of encephalopathy is the sequestration of cerebral capillaries
and venules with parasitized red blood cells (PRBCs) and non-PRBCs (NPRBCs).
Ring-like lesions in the brain are major characteristics. Risk factors include being a child under
10 years of age and living in malaria-endemic area.
Malaria
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In terminal cases blocked capillaries in the brain cause it to become swollen and
congested.
Brains of persons who die of cerebral malaria show congestion and thrombosis of
small blood vessels in the white matter, which are rimmed with edema and
hemorrhage (“ring hemorrhages”).
Malaria
• Malarial pigment can also be seen in the
capillaries; proteinaceous material may be
seen around the involved vessels
• There is necrosis of the perivascular white
matter, and focal loss of myelin staining,
also accumulation of reactive microglia
and astrocytes in the vicinity.
Dengue virus
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One-third of the world’s population living in areas at risk for transmission, dengue infection
is a leading cause of illness and death in the tropics and subtropics with 100 million people
are infected yearly.
Dengue is caused by any one of four related viruses transmitted by mosquitoes (Aedes
aegypti).
There are no vaccines to prevent infection with dengue virus (DENV).
Symptoms of dengue fever include fever, retro-orbital pain, joint pain and muscle pain –
break bone fever. The initial illness is much milder than repeat infections with the virus
Dengue
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Encephalopathy is the most common neurological manifestation. It may result from
hypotension, cerebral edema, microvascular and frank hemorrhage, hyponatremia, and
fulminant hepatic failure which may be part of Reye‘s Syndrome.
These metabolic factors are held responsible for neurological manifestations when the
virus or its serological evidence cannot be found in the CSF.
Animal studies have shown a virus mediated breakdown of the blood-brain barrier.
Measles – SSPE
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The family of Paramyxoviridae contains viruses that induce a wide range of
distinct clinical illnesses in humans.
These include measles virus, which in rare instances is followed by
subacute sclerosing panencephalitis (SSPE).
SSPE is a late complication central nervous system infection of measles
virus occurring 5 to 15 years after infection. It occurs more often in males
who developed measles early in life and causes a CNS degenerative
disease.
High levels of antibody to measles virus are found in Serum and CSF and it
is apparent that intrathecal immunoglobulin is synthesized in this disorder.
Syphilis - Leues
• Sexually-transmitted disease caused by
Treponema pallidum, a spirochetal
organism
• Often called the great imitator
Syphilis - Leues
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Primary syphilis: (Treponema pallidum), - 10 to 90 days. The first symptom of primary syphilis is
often a single, small, round, painless sore, called a chancre.
Secondary syphilis: symptoms can begin 2 to 10 weeks after the chancre sore appears. The
most common symptom is a rash on the palms of the hands and the bottoms of the feet. The
symptoms appear to resolve with or without treatment.
Latent syphilis: This stage can start from 2 years to over 30 years after the initial infection. In
late latent syphilis, the infection is quiet and the risk of infecting a sexual partner is low or
absent.
Tertiary syphilis: In this stage of syphilis, the bacteria can damage almost any part of the body,
but most commonly affects the Heart, Eyes, Brain, Nervous system, Bones and joints, liver
Syphilis - Leues
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Late neurosyphilis (brain or spinal cord damage) is one of the most severe signs of this
stage. An example of neurosyphilis is a disease called tabes dorsalis. It occurs in persons
with untreated syphilis many years after they are first infected.
Neurosyphilis is an infection of the brain or spinal cord. It occurs in persons with untreated
syphilis many years after they are first infected.
Neurosyphilis may be asymptomatic, with findings only on examination of cerebrospinal
fluid. The usual findings on exam of CSF are presence of white blood cells, elevated
protein, and a reactive serologic test for syphilis (the VDRL is generally accepted as the
standard test for CSF).
It is vital to understand that, in the presence of HIV infection, neurosyphilis in any of its
manifestations may become apparent within weeks to months of primary syphilitic infection
Syphilis - Leues
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Abnormal walk (gait)
Blindness
Confusion
Dementia
Depression
Headache
Incontinence
Inability to walk
Irritability
Loss of muscle function
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Mental decline
Paralysis
Poor concentration
Seizures
Stiff neck
Tremors
Visual disturbances
Weakness, numbness of
lower extremities
Note: There may be no
symptoms
Syphilis - Leues
• Penicillin is used to treat neurosyphilis by injection
IV daily for 10 - 14 days or with probenecid by
mouth 4 times a day, combined with daily IM -both for 10 - 14 days.
• Follow-up blood tests and lumbar punctures for
CSF fluid analysis at 3, 6, 12, and 24 to establish
cure.
Lyme disease
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Lyme disease is caused by the bacterium Borrelia burgdorferi and is transmitted to humans
by the bite of infected blacklegged ticks.
Typical symptoms include fever, headache, fatigue, and a characteristic skin rash called
erythema migrans. If left untreated, infection can spread to joints, the heart, and the
nervous system.
The organism is a spirochetal organism.
Lyme disease – 3 stages
• Stage I – early localized infection
characterized by a
bull’s-eye rash called
erythema chronicum
migrans
Lyme disease – 3 stages
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Stage II – early disseminated infection with 15% having neurologic
symptoms including Bell’s palsy. Patient may experience radiculopathies,
meningitis or mild encephalitis. Some cases of neuroborreliosis have only
altered mental status and the diagnosis may therefore be elusive.
Lyme disease
• Stage III – late persistent infection which is
characterized by:
– Polyneuropathy with abnormal sensation in hands and feet
• Mostly sensory
– Lyme encephalopathy with memory and cognitive
dysfunction
– Chronic encephalomyelitis cognitive impairment, weakness
in the legs, awkward gait, facial palsy, bladder problems,
vertigo and occasionally psychiatric disorders.
So be careful
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Don’t travel to Southwest …coccidiomycosis
Don’t eat fuzzy strawberries. … zygomycetes
Don’t rob King Tut –the curse is Aspergillus
Don’t eat undercooked mutton….Echinococcus
Don’t get dengue a second time…
Stay out of the Mississippi River Valley …Histo
Keep your contacts clean….. Acanthamoeba
Don’t eat poorly cooked pork / lamb/ beef…. Toxoplamosis
Don’t assassinate the cat…. Toxo
Only deal with potty trained birds…. Cryptococcus
Stay out of the fountain…. Naegleria fowleri
Don’t ask my daughter for answers…… I gave her all the wrong answers
Stay away from heart shaped tubs