Nervous system infections Flashcards

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1
Q

Meningitis characteristics?

A

Inflammation of the meninges (tissues surrounding the brain)
- anatomical syndrome: many different microorganisms can cause infection of meninges and all produce a similar set of symptoms
- can be caused by bacteria,viruses, or fungi
- more serious forms of meningitis are caused by bacteria
- meningitis in neonates is most often caused by different microorganisms than those that cause disease in children and adults

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2
Q

Meningitis diagnosis?

A
  • lumbar puncture/ spinal tap
  • gram stain and or culture of CSF are performed
  • treatment with broad-spectrum antibiotics started immediately
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3
Q

Meningitis signs and symptoms?

A
  • severe headache
  • painful or stiff neck
  • fever
  • nausea and vomiting
  • photophobia (sensitivity to light)
  • skin rashes may be present in specific types of meningitis
  • increased # of lymphocytes in CSF
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4
Q

Bacterial meningitis causative agent?

A

Neisseria meningitidis
- gram-negative diplococci commonly known as meningococcus
- associated with epidemic forms of meningitis
- causes the most serious form of acute meningitis (15-20% of all cases)
- most cases occur in young children bc vaccination is not recommended until 11
- infection rate in most populations is 1% indicating well developed natural immunity
- treated meningococcemial disease has a 15% mortality rate

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5
Q

Neisseria meningitidis transmission and epidemiology?

A
  • bacteria don’t survive long in the environment
  • usually acquired through close contact w/ secretions or droplets
  • sporadic or epidemic incidence in late winter/early spring
  • reservoir = humans harboring pathogen in the nasopharynx
  • carriers living in close quarters w/ susceptible individuals more readily transmit diseased
  • high risk groups = young and older children, and young adults
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6
Q

Neisseria meningitidis Diagnosis?

A
  • differential diagnosis must be done quickly
  • meningococcal meningitis must be confirmed or ruled out because it can be rapidly fatal
  • treatment is begun with this organism in mind until it is ruled out
  • bacterial meningitis is considered a medical emergency
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7
Q

Neisseria meningitidis diagnosis?

A

CSF, blood, or nasopharyngeal samples are stained and observed for characteristics of diplococci
- specific rapid tests are available for detecting capsular polysaccharides or cells directly from specimens without culturing
- Modified Thayer-Martin or chocolate agar is used for culture and incubated in a high CO2 atmosphere
- Presumptive indication of the genus obtained through gram stain and oxidase test

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8
Q

Neisseria meningitidis treatment?

A
  • vital that antibiotic therapy begins ASAP
  • high dose of penicillin G given intravenously
  • treatment for shock and intravascular clotting may also be required
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9
Q

Neisseria meningitidis prevention?

A

individuals in close contact with w/ infected patients should receive preventative therapy with rifampin or tetracycline

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10
Q

Meningoencephalitis characteristics?

A

inflammation of the brain and its protective membranes
caused by: naegleria fowleri and Acanthamoeba (amoebas)
accidental parasites that invade the body only under unusual circumstances

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11
Q

Meningoencephalitis via Naegleria fowleri characteristics?

A
  • usually aquired by people who have been swimming in warm, natural bodies of fresh water
  • amoeba is forced into nasal passages as a result of swimming, diving, or other aquatic activities
  • amoeba burrows into the nasal mucosa, multiplies, and migrates to the brain and surrounding structures
    results in PAM: primary amoebic meningoencephalitis
  • causes massive destruction of brain and spinal tissue that results in hemorrhage and coma
  • death occurs within a week
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12
Q

Meningoencephalitis via Naegleria fowleri transmission and epidemiology?

A
  • wide distribution in fresh bodies of water
  • very common; children carry the amoeba as harmless biota, especially during summer months
  • series of events leading to infection is rare
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13
Q

Meningoencephalitis via Naegleria fowleri prevention and treatment?

A
  • this meningoencephalitis advances so rapidly that treatment is usually futile
    • Early therapy with amphotericin B, sulfadiazine, or
      tetracycline in some combination can have some
      benefit
      Because of the wide distribution of the amoeba and its hardiness, no general method of control exists
      public swimming pools and baths must be adequately chlorinated and checked periodically for the amoeba
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14
Q

Prion characteristics?

A

Proteinaceous infection particles that contain no genetic material
Causes Transmissible spongiform encephalopathies (TSEs)
- neurodegenerative diseases w/ long incubation but rapid progression
- Human TSEs = Creutzfeildt-Jkob disease (CJD); Genstmann-Strussler-Scheinker disease, and fatal familial insomnia
Animal TSEs = scrapie (sheep and goats), transmissible mink encephalopathy, bovine spongiform encephalopathy (BSE/mad cow disease)

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15
Q

Prion CJD causative agent?

A

Prions cause transformation of normal host protein PrP that functions in normal brain development
- mutation causes a structural change in the protein, making PrP catalytic and able to convert other normal PrP proteins into the abnormal form
- self-propagating chain reaction leads to accumulation of altered PrP, plaques, and spongiform damage (holes in brian)

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16
Q

Prion CJD signs and symptoms?

A
  • altered behavior, dementia, memory loss, impaired senses, delirium, and premature senility
  • Uncontrollable muscle contractions continue until death, usually within a year of diagnosis
17
Q

Prions transmissibility?

A

considered transmissible agents
- PrP proteins can be acquired through transmission
- genetic mutations of the PrP gene can also be passed on as heritable traits
- Prions are hardy; resistant to chemicals, radiation, heat, and prolonged autoclaving

18
Q

Prions CJD epidemiology?

A
  • in late 90s, humans contracted vCJD after injecting meat from cattle infected with BSE
  • cases of transmission of CJD via contaminated surgical instruments have been found
  • normal disinfection and sterilization are not sufficient to eliminate prions from instruments and surfaces
19
Q

Rabies characteristics?

A

slow progressive zoonotic disease
- characterized by fatal encephalitis
- distinct pathogenesis and symptoms
Distributed almost worldwide

20
Q

Rabies signs and symptoms?

A

Incubation period of 1-2 months or more (depends on wound site, severity, and inoculation dose)
- shorter incubation with facial, scalp, or neck wounds (closer to the brian = less incubation)
Prodromal phase:
- fever, nausea, vomiting, headache, fatigue, and other nonspecific symptoms
Handful of patients have recovered in recent years from long term treatment but usually fatal

21
Q

Rabies Transmission?

A

Primary reservoirs are wild animals but both wild and domestic animals spread disease through bites, scratches, and inhalation of droplets
- majority transmitted to humans from bats
- majority US cases occur in rabies occur in wild animals

22
Q

Rabies epidemiology?

A

Animal reservoirs vary in the US (usually raccoons, bats and skunks)
- regional differences in the dominant reservoirs
- Skunks = California
- raccoons = East
- Foxes = Texas

23
Q

Rabies Diagnosis?

A
  • Reverse transcription PCR used (saliva sample)
  • Must be accompanied by the detection of antibodies to the virus in serum or spinal fluid
  • skin biopsies are also used
24
Q

Rabies prevention and treatment?

A

BIte from wild or stray animal means animal must be assessed, meticulous wound care, and combination of passive and active postexposure immunization
- wound is infused with human rabies immune globulin (HRIG) to impede the speed of the virus
- Globulin also injected intramuscularly to provide immediate systemic protection
- full vaccination course is started

High-risk groups such as vets, animal handles, lab personnel, and travelers receive 3 doses of vaccine to protect

25
Q

Tetanus characteristics and causative agent?

A

Neuromuscular disease (also known as “lockjaw”)
- caused by Clostridium Tetani
- common resident of cultivated soil and
gastrointestinal tract of animals
- Gram-positive, endospore-forming bacillus
- endospores often swell in vegetative cells
- spores only produced under anaerobic conditions

25
Q

Tetanus characteristics and causative agent?

A

Neuromuscular disease (also known as “lockjaw”)
- caused by Clostridium Tetani
- common resident of cultivated soil and
gastrointestinal tract of animals
- Gram-positive, endospore-forming bacillus
- endospores often swell in vegetative cells
- spores only produced under anaerobic conditions

26
Q

Tetanus signs and symptoms?

A

First symptoms are clenching of jaw, followed by arching of back, flexion of arms, and extension of legs
- caused by Tetanospasmin (neurotoxin released by bacteria) that binds to target sites on peripheral motor neurons, spinal cord and brain, and in sympathetic nervous system
- toxin blocks the inhibition of muscle contraction, causing muscles to contract uncontrollably

Risis sardonicus: AKA “sardonic grin” conferred by lockjaw (looks like smiling)
- death most often occurs due to paralysis of the respiratory muscles

27
Q

Tetanus pathogenesis and virulence factors?

A
  • presence of endospores in a wound is not sufficient to initiate infection
    • unable to invade damaged tissues readily
    • organism is anaerobic and endospores cannot
      become established unless tissue is necrotic/has
      poor blood supply
      As vegetative cells grow tetanospasmin is released into the infection site and spread
28
Q

Tetanus transmission and epidemiology?

A

Endospores enter the body through puncture wounds, burns, umbilical stumps, frostbite, crushed body part
- most cases of tetanus occur among geriatric patients and IV drug users
- Historically maternal & neonatal tetanus cases high but was improvised with more hygienic delivery practices and vaccination

29
Q

Tetanus treatment?

A
  • patient w/ clinical appearance should receive immediate antitoxin therapy w human tetanus immune globulin (TIG) and penicillin G
30
Q

Tetanus prevention?

A

Recommended vaccination series:
* 1- to 3-month-old babies consists of three injections given 2 months apart, followed by boosters at 1 and 4 years
* Protection lasts 10 years
* Pregnant women should be vaccinated
* Toxoid with TIG should be given to injured persons who have never been immunized or whose last booster was received more than 10 years previously

31
Q

Botulism characteristics?

A

intoxication caused by an exotoxin associated with eating poorly preserved foods
- can also occur as a true infection
- modern techniques of food preservation and medical treatment reduce the incidence and mortality rate

32
Q

What are the 3 forms of botulism?

A

infant
food-borne
wound

33
Q

Botulism signs and symptoms?

A

Botulinum (neurotoxin produced by C. botulinum) results in flaccid paralysis, a loss of ability to contract muscles

Early symptoms:
- double vision, difficulty swallowing, dizziness, no sensory or mental lapse
Later symptoms:
- descending muscular paralysis, respiratory compromise
- death usually results from respiratory arrest ( mechanical respirators have reduced fatality to 10%)

34
Q

Botulism causative agent?

A

Clostridium botulinum
- endospore-forming anaerobe
- does damage through the release of an exotoxin
- species has 7 types that vary in distributions among animals, regions, and types of exotoxin

35
Q

Botulism culture and diagnosis?

A
  • Diagnostic standards are different for 3 presentations
  • CDC and state health department need to be notified if a case is suspected
36
Q

Botulism prevention and treatment?

A
  • Antitoxin provided by CDC soon after diagnosis can prevent worst outcomes of disease
  • patients are managed w/ respiratory and cardiac support systems
  • hospitalization required in all cases
  • recovery takes weeks (5% mortality rate)