LEC-7 Bacterial Meningitis Flashcards by Blake Hollowoa

What is aseptic meningitis?

Meningeal inflammation with negative bacterial cultures

Starts as acute inflammation, and progresses to mononuclear infiltration

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What are the viral agents that cause aseptic meningitis?

Enteroviruses (Coxsackie, echovirus, other non-polioviruse enteroviruses) - Most common cause

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What are the fungal agents that cause aseptic meningitis?

Cryptococcus, Coccidiodies

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What are the bacterial agents that cause aseptic meningitis?

Mycobacterium tuberculosis
Treponema pallidum
Borrelia burgdorferi

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What is the most common cause of bacterial meningitis up to 3 months of age?

Group B Sreptococcus

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What is the most common cause of bacterial meningitis between 3 months and 3 years of age?

Streptococcus pneumoniae

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What is the most common cause of bacterial meningitis between 3 years and 10 years of age?

Streptococcus pneumoniae

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What is the most common cause of bacterial meningitis between 10 years and 19 years of age?

Neisseria meningitidis

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What is the most common cause of bacterial meningitis for adults (20 and above)?

Streptococcus pneumoniae

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What are the clinical signs and symptoms of bacterial meningitis? (specifically Neisseria meningitidis)

Petechiae (1-3 days; not absolute so don’t rule out if absent)
Headache, fever
Listless (neurological sign)
Cervical rigidity
Positive BC for an oxidase-positive Gram-neg diplococcus

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What is Brudzinski’s sign?

Sign of cervical rigidity

Lifting head while patient is supine (if positive knees will come up)

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What is Kernig’s sign?

Hamstring spasm that occurs when you try to straighten knee with leg at 90 degree angle from supine)

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A Neiserria meningitidis infection may invade and colonize the oropharynx, resulting in _________________.

Pharyngitis (mild)

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What may develop after pharyngitis caused by N. meningitidis?

Bacteremia - Transient present of oragnism in blod

URTI (still fairly mild)
Positive blood culture
Transient with fever, malaise
Resolves in 1-2 days usually

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Following bactermia, N. meningitidis may invade the blood, resulting in meningococcemia. What clinical signs and symptoms are seen in this condition?

I. Positive blood culture (growth of organism in blood)
II. Malaise
III. Fever
IV. May resolve or proceed further

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Following meningococcemia, what can result if the disease doesn’t resolve?

Meningitis!! (medical emergency)

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What are the signs and symptoms of meningitis?

Sudden onset of fever, nausea, vomiting, headache, decreased ability to concentrate
Meningococcemia (may be present)
Brudzinki's sign
Kernig's sign
Petechia
Neck stiffness
May develop into meningoencephalitis
Disseminated intravascular coagulation (DIC) or shock

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What are the clinical signs and symptoms of Disseminated Intravascular Coagulation (DIC)?

High fever, chills, myalgia, nausea, vomiting, headache

Can result in septic shock; increased vascular permeability; fluid loss

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What is the cause of Disseminated Intravascular Coagulation (DIC)?

Macrophage production of tissue factor

Results in widespread ischemic changes and bleeding to using up all clotting factors

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What is Waterhouse-Friderichsen syndrome?

Adrenal infarction leading to acute adrenal insufficiency

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What are the signs and symptoms of Waterhouse-Friderichsen syndrome?

Widespread petechial rash
Meningitis is absent
Death may occur due to pulmonary insufficiency
Hemorrhage into adrenal glands results in failure
Associated with DIC

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What is the reservoir for N. meningitidis?

Nasopharynx

What months are highest for N. meningitidis attacks?

February and March

Of the N. meningitidis serogroups, Serogroup __ is responsible for 50-55% of all infection cases in the US.

Serogroup B

The __________ of N. meningitidis is responsible for its resistance to phagocytosis and a great deal of its virulence.

Capsule

N. meningitidis possesses ______ that allow it to adhere to mucosal cells and reside in the nasopharynx.

Pili

N. meningitidis possesses ___________________ in its outer membrane. This is an LPS-like molecule that lacks O-antigens in its sidechains.

Lipooligosaccharide (LOS)

________________ is necessary for definitive diagnosis of N. meningitidis infection.

Bacterial culture

(T/F) A vaccine for N. meningitidis serogroups A, B, C, Y, and W exists in the US.

False. A, C, Y, and W exists in the US, while B vaccine is licensed in Europe only. Clinical trials are currently underway in the US.

What is the shape of N. meningitidis?

Kidney bean-shaped diplococci

N. meningitidis cultures test oxidase (positive/negative).

Positive. N. meningitidis possess a cytochrome oxidase system

N. meningitidis may be cultured most easily on ________ and ________ agar.

Blood and chocolate agar

N. meningitidis possesses an (IgG/IgM/IgA/IgD/IgE) protease.

IgA protease

The lipooligosaccharide (LOS) of N. meningitidis activates macrophages through the _________ pathway.

Toll

Production of ________ from activated macrophages results in vascular permeability, hemorrhage, and petechiae.

TNF-α

What is the treatment for N. meningitidis?

Vancomycin | Cefotaxime (3rd gen cephalosporins)

What is the prophylactic treatment for N. meningitids?

Rifampin and ciprofloxaxin

The definitive host of Toxoplasma gondii is the _______, while ________ is an accidental host.

Cat is definitive host | Man is accidental host

What is the life cycle of Toxoplasma gondii in a cat?

I. Sexual and asexual reproduction in gut of cat II. Upon ingestion of bacterial oocyst, sporozoites released that infect intestinal epithelial cells III. Produces tachyzoites which infect other epithelial cells in gut of cat to continue life cycle. Some tachyzoites may move to other tissues, forming pseudocysts that contain bradyzoites IV. Some tachyzoites develop into male and female gametes and unite to form oocyst V. Oocysts passed in stool and may be consumed by other cats VI. Recycle to step II

What is the life cycle of Toxoplasma gondii in mammals other than a cat?

I. Oocysts are ingested II. Sporozoites emerge from oocysts and develop into tachyzoites III. Tachyzoites enter circulation, become systemic, and infect cells in other parts of body including: liver, lung, spleen, muscles, and brain. IV. Tachyzoites asexually (sexual not possible in mammals other than cat) reproduce, kill host cell, and spread to other cells V. Some move to other tissues and form pseudocysts containing bradyzoites

What types of patients are most commonly infected with Toxoplasmosis gondii?

Immunocompromised patients (80-90% of immunocompetent patients are asymptomatic)

What symptoms are seen in acute toxoplasmosis?

I. Lymphadenopathy II. Muscle pain III. Malaise, fever, chills IV. Chorioretinitis (inflammation of choroid and retina of eye) V. Resembles infectious mononucleosis on slides

What symptoms are seen in severe acute toxoplasmosis?

I. Hepatitis II. Encephalomyelitis (inflammation of brain and spinal cord) III. Myocarditis

Toxoplasmosis is more severe in (immunocompromised/immunocompetent) patients.

Immunocompromised

Toxoplasmosis usually manifests in the form of a disease of the _________________

Central nervous system - Encephalopathy - Meningoencephalitis

Congenital toxoplasmosis in the (first/second/third) trimester typically results in spontaneous abortion, stillbirth, or severe disease in the newborn.

First trimester

Congenital toxoplasmosis in the (first and second/second and third/first and third) trimesters may result in epilepsy, encephalitis, hydrocephalus, psychomotor disorders, retardation, or chorioretinitis.

Second and third trimesters

For diagnosis of acute toxoplasmosis, a __-fold increase in serological titer is necessary.

4-fold

What is the treatment for toxoplasmosis?

Sulfadiazine and pyrimethamine

_______________ is a free-living amebo-flagellate in soil and water. It enters humans by opportunistic infection. It infects through penetration of the cribriform plate through the nose and entry into the brain where it produces meningoencephalitis. It then results in severe frontal headache, fever, and lethargy which rapidly progresses to confusion, convulsions, and coma. It is often fatal in 6-17 days. It is diagnosed by detection of amoeba in purulent CSF of the patient.

Naegleria fowleri

Naegleria fowleri is most often found in _________________.

Warm, fresh water bodies and mud

What is the typical treatment when infection by Naegleria fowleri is suspected?

FARM-D ``` Fluconazole Amphotericin Rifampin Milte-fosine Dexamethasone ``` Also, cooling of the patient to 33C

______________ is a free-living amebo-flagellate in soil and water. It causes CNS infection through penetration of the cribriform plate. It displays a longer infection course than Naegleria fowleri, and may also result in ocular infection through contaminated contact lenses or dirt in eyes.

Acanthamoeba

What are the signs and symptoms of Naegleria fowleri infection?

Signs and symptoms of meningitis Amoebae detected in wet mount Visualized with Wright stain