Transcript chapter_19-20_rjc_8-29-11-Infectious Diseases of Skin, Eye

Chapter 19
Infectious Diseases Affecting the Skin
Skin
• Epidermis
– Stratum corneum (dead cells are sloughed
off)
• Keratin (protein)
– Waterproof the skin
– Protects from microbial invasion
– Replaced every 25-45 days
– No nerve endings or blood vessels
Skin continued
• Dermis
– Source for epidermis cells
– Connective tissue (fibers)
– Nerves, blood vessels, lymphatic
– Hair follicles, glands (sebum, lysozyme)
• Subcutaneous layer
The different layers of the skin are important defenses
of the skin.
Fig. 18.1 A cross-section of skin
Normal flora
• Survive dry and salty conditions
• Dense populations in the skin folds
• Types
– Diphtheroids (Propionbacterium acnes)
– Micrococci (Staphylococcus epidermis)
– Yeast (Candida albicans)
Structure of the Skin
• Wounds
– Trauma to any tissue of the body
• Cuts, scrapes, surgery, burns, bites, etc.
– Allow microbes to infect the deeper tissues
of the body
• In most cases other body defenses eliminate
infection
• Can result in severe or fatal diseases
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Skin Diseases
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Acne
Impetigo
Cellulitis
Staphylococcal Scalded Skin Syndrome (SSSS)
Gas gangrene
Hansen’s Disease
Skin rashes
Warts
Large skin lesions
Acne
• Most common skin disorder
• Proprionibacterium acnes, actually part of normal
flora
• Increased sebum production, ducts become
blocked, rupture of follicle lining.
• Prevention: good skin hygiene, genetic.
• Rx- antibiotics, Accutane, topicals with benzoyl
peroxide, Retin-A.
• New treatment uses blue-light wavelength to
destroy bacteria
Figure 19.7 The development of acne
Normal skin
Pore
Oily sebum produced by
glands reaches the hair
follicle and is discharged
onto the skin surface via
the pore.
Bacteria
Sebum
Sebaceous
gland
Hair
follicle
Whitehead
Inflamed skin swells over
the pore when bacteria
infect the hair follicle,
causing the accumulation
of colonizing bacteria and
sebum.
Blocked
pore
Blackhead
Pus
Pustule formation
Dead and dying bacteria
and sebum form a blockage
of the pore.
Severe inflammation of the
hair follicle causes pustule
formation and rupture,
producing cystic acne,
which is often resolved by
scar tissue formation.
Boils: Furuncles and Carbuncles
Carbuncles- multiple heads,
Furuncles- one head
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AKA Folliculitis, boils, sty (eyelash follicle)
Infection of hair follicles
Caused by S. aureus most often
Spread by direct contact through micro
abrasions
• Complications; septicemia, pain, pressure
• Prevent with cleanliness, no sharing of
fomites
• Rx- drainage, antibiotics
Figure 19.2 Staphylococcus
Impetigo
• Caused by S. pyogenes and S. aureus
• Direct/indirect contact through breaks in the skin, easily
spread through fomites
• Most common in school age children
• Symptoms: superficial, pus filled blisters covered by yellowish
brown crust, weepy. “brown sugar crusts”
• Highly contagious
• Prevention; hand washing, clean towels, bedding etc.
• Rx- topical antibiotics, oral antibiotics for more severe cases
Scalded skin
syndrome
• Caused by exfoliative exotoxin released by
lysogenized strains of S. aureus
• More common in infants, local infection
spreads through the blood.
• Skin blisters, then begins to peel. Red moist,
tender skin revealed underneith
– 20-100% of epidermis peels off in sheets,
– Fatigue, fever, malaise, irritability
– Rx- antibiotics, fluid & electrolyte replacement.
Bacterial Diseases of the Skin and
Wounds
• Necrotizing Fasciitis
– Pathogen and virulence factors
• Most cases caused by S. pyogenes
• Various enzymes facilitate invasion of tissues
• Exotoxin A and streptolysin S are also secreted
– Pathogenesis and epidemiology
• S. pyogenes enters through breaks in the skin
• Usually spread person-to-person
– Diagnosis, treatment, and prevention
• Early diagnosis is difficult because symptoms are
nonspecific
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• Treat with clindamycin and penicillin
Figure 19.6 Necrotizing fasciitis
Bacterial Diseases of the Skin and
Wounds
• Cat Scratch Disease
– Pathogen and virulence factors
• Caused by the Gram-negative bacterium
Bartonella henselae
• Endotoxin is the primary virulence factor
– Pathogenesis and epidemiology
• Transmitted by cat bites or scratches
– Diagnosis, treatment, and prevention
• Diagnosed with serological testing
• Treated with antimicrobials
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Bacterial Diseases of the Skin
and Wounds
• Pseudomonas Infection
– Pathogen and virulence factors
• Pseudomonas aeruginosa is the causative agent
– Found in soil, decaying matter, moist environments
• Virulence factors
– Adhesins, toxins, and a polysaccharide capsule
– Pathogenesis
• Infection can occur in burn victims
– Bacteria grow under the surface of the burn
• The bacteria kills cells, destroys tissue, and
triggers shock
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Figure 19.8 Pseudomonas aeruginosa infection
Gangrene
• Gas gangrene, caused by Clostridium perfringens
toxin. (anaerobic bacteria)
• Often associated with crushing, or dirty wounds,
extensive tissue damage,
C. perfringens is transferred into wound.
• Acute onset of pain, fever, skin turns bluish and tight
because of gas production, brown frothy rotten
smelling fluid in wound. Sepsis is likely. Necrosis of
tissue. Crackling sound.
• Prevention- prompt cleaning of wounds.
• Rx- antibiotics, hyperbaric oxygen treatments,
debridement, amputation.
Bacterial Diseases of the Skin and
Wounds
• Gas Gangrene
– Pathogenesis and epidemiology
• Traumatic event must introduce endospores into
dead tissue
• Mortality rate exceeds 40%
– Diagnosis, treatment, and prevention
• Appearance is usually diagnostic
• Rapid treatment is crucial
– Surgical removal of dead tissue
– Administration of antitoxin and penicillin
• Prevent with proper cleaning of wounds
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Leprosy, Hanson’s disease
• Caused by Mycobacterium leprae. Slowly grows at
cooler temperatures (30o C.) (what body parts does it
strike?)
• After several years of infection symptoms finally
develop, skin lesions. Develops into tuberculoid, or
lepromatous variety.
• Tuberculoid destroys tissue, but mostly lose of
nervous sensation in those areas.
• Lepromatous destroys a lot of tissue. Underlying
bone and cartilage often destroyed. Loss of sensation
patchy.
• Rx- Dapsone, rifampin, clofazimine, Hawaii treatment
Chicken Pox
• Varicella zoster virus
• Highly contagious, direct/indirect transmission
through respiratory droplets, and weepy
lesions.
• Pathology
– Macules (red spots) become papules (bumps)
turn into vesicles (blisters) become infected and
turn into pustules.
– Itchy rash spreads from head, down to trunk,
then out to extremities. Concentrated on trunk.
– Rx.- Vaccination, supportive therapy, calamine
lotion
Viral Diseases of the Skin and
Wounds
• Chickenpox and Shingles
– Signs and symptoms
• Chickenpox characterized by lesions on the back
and trunk that spread across body
• Shingles lesions localized to skin along an infected
nerve
– Pathogen
• Varicella-zoster virus (VZV) causes both diseases
– Pathogenesis
• Infected dermal cells cause rash characteristic of
chickenpox
• Virus becomes latent in nerve ganglia
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– Reactivated VZV causes shingles
Viral Diseases of the Skin and
Wounds
• Chickenpox and Shingles
– Epidemiology
• Chickenpox occurs mostly in children
– Disease is more severe in adults
• Risk of shingles increases with age
– Diagnosis, treatment, and prevention
• Diagnosis based on characteristic lesions
• Treatment based on relief of symptoms
• Vaccine available against chickenpox
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Cold sores
Figure 1. The herpes simplex virus life cycle. (a) Herpes simplex virus (HSV) is shown
undergoing the lytic cycle (entry, uncoating, viral transcription and DNA replication in the nucleus,
particle assembly, exit from the cell) in epithelial cells of the skin to cause a primary infection. (b)
Some virus enters the sensory neuron terminals and travels retrogradely to the nucleus where it
establishes latency. (c) Periodic reactivation results in anterograde transport of viral particles,
shedding from the neuron, and re-infection of epithelial cells, which leads to asymptomatic
shedding or recurrent lesions.
• Herpes simplex I, Cold sores, fever blisters, oral
herpes
• Majority of population infected, only 15% have
outbreaks
• Transmission- fomites, and direct contact
• Virus remains in dorsal root ganglia, reactivated by
several factors; stress, excessive sun, heat,
immunodeficiency.
• Prevention, avoid close contact with someone who
has an outbreak
• Rx-acyclovir reduces length and severity of outbreaks
Figure 19.12 Sites of events in herpesvirus infections
Ophthalmic branch
Trigeminal (V)
nerve ganglion
Site of viral latency
Ocular herpes
Maxillary branch
Mandibular branch
Brachial ganglia
Site of viral latency
Fever blisters
Sacral ganglia
Site of viral latency
Genital
herpes
Whitlow
Smallpox
• Variola virus (overall fatality 30%)
• Transmission - Fairly prolonged face to face contact,
as well as contact with body fluids or infected items
like bedding.
• Fever, headache, body ache, then rash appears in
the mouth. Rash moves to head and extremities.
Red spots become umbilicated bumps with thick fluid
inside. Then pustules with hard bump inside, then
scab over.
• Infectious until scabs have all fallen off.
• Last case in U.S. 1949, last case in the world 1977
eradicated through vaccination.
• Cidofovir possible drug for treatment
Measles, rubeola
Measles, Rubeola (red measles)
• Rubeola virus
• Transmitted by respiratory droplets
• More common and less severe in school aged
kids vs, infants or adults.
• Pathology
– Fever, runny nose cough swollen weepy eyes
– Koplik spots appear on tongue and inside of
mouth (salt grains)
– Eruption of fine red rash on the forehead and
spreads to the trunk of body.
– Rx- MMR vaccine 95-99% effective, could be
eradicated if not for unvaccinated population.
Cases
Cases (thousands)
Figure 19.15 Measles cases in the United States since 1950
Attenuated
vaccine licensed
Year
Rubella, German measles
• Rubella virus
• Transmission respiratory droplets
• Mild childhood disease, headache fever,
malaise, rash on face, chest, abdomen,
NO koplik spots
• Serious complication for pregnant women,
– Infection during 1st 6 weeks minor deafness, crosses
the placenta can affect, ears, eyes, heart and brain.
Rx- MMR vaccine very effective, 3 months before
pregnancy test your titer.
Figure 19.14 The efficacy of immunization against rubella
Cases
Cases (thousands)
Attenuated
vaccine licensed
Year
Features for measles, rubella, fifth disease, and
roseola.
Checkpoint 18.8 Maculopapular rach diseases
Viral Diseases of the Skin and
Wounds
• Warts
– Benign epithelial growths on the skin or
mucous membranes
• Can form on many body surfaces
– Various papillomaviruses cause warts
– Most warts are harmless
– Transmitted via direct contact and fomites
– Diagnosed by observation
– Various techniques to remove warts
• New warts can develop due to latent viruses
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Figure 19.13 Various kinds of warts--lesions caused by papillomavirusesoverview
Features of papillomas and molluscum contagiosum.
Checkpoint 18.9 Wart and wart-like eruptions.
Features of leishmaniasis and cutaneous anthrax.
Checkpoint 18.10 large pustula skin lesions
Superficial mycoses
Mycoses of the Hair, Nails, and
Skin
• Mycoses are diseases caused by fungi
• Most are opportunistic pathogens
• Mycoses are classified by infection
location
– Superficial – occur on the hair, nails, and
outer skin layers; most common fungal
infections
– Subcutaneous – in the hypodermis and
muscles
– Systemic – affect numerous systems
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• Tinea corporis (skin/ring worm), capitis (scalp), cruris
(groin), pedis (foot)
- Caused by various dermatophytes
• Transmission through breaks in the skin, spread with
contact.
• reddened raised area with itchy, scaly sometimes
flaking skin. Hair loss, or cracks in skin can occur.
• Prevention; reduce body surface moisture, wear
loose breathable clothing, regularly change socks,
wear flip flops at the gym!
• Rx – prescription and OTC fungal medications,
miconazole.
Figure 19.19 Dermatophytosis (ringworm)
Parasitic Infestations of the Skin
• Leishmaniasis
– Signs and symptoms
• Cutaneous: Produces large painless skin lesions
• Mucocutaneous: Skin lesions enlarge to
encompass mucous membranes
• Visceral: Parasite is spread by macrophages
throughout body
– Pathogen and virulence factors
• Leishmania is the causative agent
– Protozoan transmitted to humans by female
sand flies
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Figure 19.24 Mucocutaneous leishmaniasis
Chapter 20
Microbial Diseases of the
Nervous System
and Eyes
Eye
• Conjunctiva
– Thin membrane that covers the eye, except the
cornea
– Secretes oil and mucous-containing fluids
• Best defense
• Cornea
– Covers the iris
– Several layers of epithelial cells
– Epithelial cells can regenerate if damaged
• No lymphocytes, no inflammation
– Immune privilege
The main parts of the eye that are important eye
defenses.
Fig. 18.2 The anatomy of the eye.
The best defense of the eye is the film of tears, which
originates from the lacrimal apparatus of the eye.
Fig. 18.3 The lacrimal apparatus of the eye.
Conjunctivitis “Pink eye”
Many organisms: Neisseria, Chlamydia, Staph. & Strep.
Various viruses
Direct contact transmission
Inflammation of the conjunctiva, itching, burning, swelling
of lids, redness of eyes and eyelid, and crusty exudates.
Treatment: antibiotic therapy/ self resolution
Often associated with ear / respiratory infections
Otitis media
• Middle ear infection
• Variety of bacteria, S. pneumoniae,
S. pyogenes, S. aureus
• Associated with pink eye,
and sinusitis
• Pressure pain in ear,
rupture of eardrum
• Mastoiditis and meningitis
• Treatment with antibiotics
tubes (kids)
Summary of diseases of the skin and eye.
Taxanomic organization of microorganisms causing
diseases of the skin and eyes.
Infectious Diseases Affecting the Skin and Eyes.
Fig. 18.p573
Nervous system
• Central nervous system (CNS)
• Peripheral nerves (PNS)
CNS
• Brain
• Spinal cord
• Neurons – cells that make-up the brain
and spinal cord
• Defenses
Defenses
• Meninges – surround the brain and spinal
cord
• Cerebrospinal fluid (CSF)
• Bone casing
• Blood-brain barrier
• Immunologically privileged
A diagram of the central nervous system and the
peripheral nerves.
Fig. 19.1 Nervous system.
Important structures of the brain and spinal cord that
are associated with defenses.
Fig. 19.2 Detailed anatomy of the brain an spinal cord.
Normal flora
• Absent
• Viruses can exist in a dormant state in the
nervous system
Structure of the Nervous System
• Portals of Infection of the Central
Nervous System
– CNS is an axenic environment
• It has no normal microbiota
– Pathogens may access the CNS several ways
• Breaks in the bones and meninges
• Medical procedures
• Travel in peripheral neurons to the CNS
• Infect and kill cells of the meninges, causing
meningitis
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Nervous System Diseases
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Meningitis
Neonatal meningitis
Meningoencephalitis
Acute encephalitis
Subacute encephalitis
Rabies
Poliomyelitis
Tetanus
Botulism
African sleeping sickness
Bacterial Diseases of the
Nervous System
• Bacteria cause disease in two ways
– Infect cells of the nervous system
• Meningitis
• Leprosy
– Bacteria growing elsewhere release toxins
that affect neurons
• Botulism
• Tetanus
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Meningitis
• Five species cause 90% of bacterial meningitis cases
– Neisseria meningitidis (most severe)
– Streptococcus pneumoniae (most common in adults)
– Haemophilus influenzae
– Listeria monocytogenes
– Streptococcus agalactiae
Also caused by various fungi and viruses.
Acute onset of fever, headache, painful or stiff neck,
increased number of white blood cells in CSF.
Confused or disturbed brain function.
Transmission – Mostly respiratory droplets
Meningococcal meningitis causes the most severe
Acute forms of meningitis. Associated with
epidemic forms of meningitis.
Petechiae, ecchymosis, shock and coma. Death can
occur within a few hours
Treatment – Suspicion of bacterial meningitis is a
medical emergency and treatment begins
immediately. 15% mortality rate for treated cases.
Penicillin is given in large doses via IV.
Vaccination is available for bacterial forms.
Viral forms:
Generally milder than bacterial or fungal forms. Usually
resolves in 2 weeks.
Prevention – good hygiene, no treatment.
Meningitis
Bacterial Diseases of the Nervous
System
• Bacterial Meningitis
– Pathogenesis
• S. agalactiae acquired during birth
• Listeria transmitted via contaminated food
• Other species transmitted via respiratory droplets
– Epidemiology
• S. pneumoniae present in throat of 75% of
humans
• Not spread by casual contact
• Meningococcal meningitis can become epidemic
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Features of meningitis caused by different species of
bacteria, and viruses.
Checkpoint 19.1 Meningitis
Viral Diseases of the Nervous
System
• Viruses more readily cross the
blood-brain barrier
• Occur more frequently than
bacterial and fungal infections
• Include meningitis, polio, rabies,
and encephalitis
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Acute encephalitis
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Viral infection
Arboviruses
Herpes simplex 1 or 2
JC virus
Viral Diseases of the Nervous
System
• Arboviral Encephalitis
– Arboviruses are arthropod-borne viruses
• Transmitted via blood-sucking arthropods
(e.g., mosquitoes)
– Mosquito-borne arboviruses can cause
arboviral encephalitis
– As zoonotic diseases, they rarely affect
humans
– Arboviruses usually cause mild, coldlike
symptoms
• Can cause if cross the blood-brain barrier
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Table 20.2 Characteristics of Arboviral Encephalitis Diseases and Viruses in
the United States
Figure 20.16 Human West Nile virus encephalitis in the United States
Reported cases
Number of reported cases
Annual deaths
(299)
(124)
(264)
(84)
(86)
(9)
Time (months/years)
(43)
(30)
Viral Diseases of the Nervous
System
• Arboviral Encephalitis
– Diagnosis based on signs and symptoms
• Confirmed by presence of arbovirus-specific
antibodies in CSF
– Treatment is supportive
– Prevention involves limiting contact with
mosquitoes
• Use netting and insect repellents
• Eliminate stagnant water
– Vaccines for horses available against EEE,
WEE, VEE, and WNV
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Subacute encephalitis
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Mostly a protozoan infection
Viral infection
Prion infection
Symptoms develop slowly
Kuru - a rare and fatal brain disorder
- occurred at epidemic levels during the 1950s-60s
among the Fore people in New Guinea.
-practice ritualistic cannibalism: relatives consumed
the tissues (including brain) of deceased family
members. Brain tissue from individuals
with kuru was highly infectious
Comparison between a normal and prion infected brain
tissue sample.
Fig. 19.14 The microscopic effects of spongiform
Encephalopathy.
Prion Disease
• A prion is an infectious protein
• Spongiform encephalopathies
• A class of diseases that includes scrapie and
mad cow disease
• Leave the brains of victims full of holes
• Humans can contract by eating meat from
infected cattle
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Prion Disease
• Variant Creutzfeldt-Jakob Disease
– Signs and symptoms
• Insomnia, weight loss, and memory failure
• Progressive worsening of muscle control
– Pathogen, pathogenesis, and epidemiology
• Caused by abnormal form of prion
• Prions may remain formant for many years
– Diagnosis, treatment, and prevention
• Diagnosed by characteristic signs and symptoms
– Confused with other forms of dementia in elderly
• No treatment is available
• Prevented by avoiding prion contaminated meat
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Rabies - rabies virus
Transmission – contact with infected body fluids,
usually animal bite. Incubation of 1-2 months
(depending on wound site).
- Virus replicates in muscle cells and then moves into
neurons (Postmortem detection of Negri bodies in the brain)
Symptoms – Anxiety, nervousness, impaired
swallowing, coma, then death.
Furious rabies - agitation, disorientation, seizures,
severe pain during swallowing = hydrophobia
Dumb rabies – paralyzed, disoriented, stuporous
Both result in coma, death from cardiac or respiratory arrest
Prevention/treatment – immunizing pets and people. Post
exposure antibody therapy and immunization.
Immunizing wild populations.
Figure 20.12 Predominant wildlife reservoirs for rabies in the U.S.
Skunk
Fox
Raccoon
Figure 20.13 Negri bodies
Negri bodies
Poliomyelitis - Poliovirus
Transmission – Fecal to oral route (Transmitted most often by drinking
contaminated water)
Symptoms are dependent upon destruction of nervous tissue.
– Signs and symptoms
• Asymptomatic infections – almost 90% of cases
• Minor polio – nonspecific symptoms; fever, headache,
nausea
• Nonparalytic polio – muscle spasms and back pain
• Paralytic polio – produces paralysis; causes degrees of
flaccid paralysis over a few hours to several days.
– Unused muscles begin to atrophy, growth slows and
deformities can develop. Limbs are often painful.
Treatment – alleviate pain, artificial ventilator if
needed, prompt physical therapy.
Prevention:
1955 Salk vaccine IPV (inactivated)
1961 Sabin OPV (attenuated) has been discontinued
in the U.S.
WHO is fighting hard to eradicate polio. Only 4
countries left with wild virus.
1988 – 350,000+ cases in 125 countries.
2005 – 1,951 cases in 4 countries.
Figure 20.11 Poliomyelitis-overview
The poliovirus has a unique icosahedral capsid shell.
Fig. 19.18 Typical structure of a picornavirus.
Tetanus - Clostridium tetani toxin (tetanospasmin)
Symptoms:
Toxin blocks the inhibition of muscle contraction.
Clenching of the jaw, extreme arching of the back.
Flexion of the arms, extension of legs.
Rigid “spastic” paralysis, death occurs because of
paralysis of respiratory muscles.
Clostridium tetani, the causative agent of tetanus, have
a unique tennis racket morphology.
Fig. 19.21 C. tetani
Transmission – wound infection, Anaerobic conditions,
necrotic tissue, poor blood supply, a dirty puncture
wound.
Prevention/treatment – toxoid vaccination, antitoxin
antibodies, antibiotics, muscle relaxants
Botulism - Clostridium botulinum toxin
3 types – food borne (intoxication), infant, or wound
(infections)
Prevents the release of acetylcholine, thus prevents
muscle contraction.
Symptoms – Double vision, dizziness, difficulty in
swallowing. Descending muscular paralysis. Death
comes from respiratory arrest. Flaccid “rag doll”
paralysis.
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Transmission – 20-25% of cases associated with low
acid vegetables and fruits improperly canned
Prevention/treatment – Proper food prep. Treat with antitoxin and cardiac and respiratory supportive care.
Recovery takes weeks.
Infant botulism – 80% of cases. Normal flora is
undeveloped. Raw honey is one suspected culprit.
Botulin can prevent the release of acetylcholine, thereby
muscle contractions do not occur.
Fig. 19.24 The physiological effects of botulism toxin.
African Trypanosomiasis (sleeping sickness)
2 protists, Trypanosoma brucei gambiense and
Trypanosoma brucei rhodesiense cause the
disease.
Transmitted by the Tse Tse fly in equatorial Africa.
Migrate from bite site to secondary lymph tissue,
and multiply – fever, malaise, enlarged nodes,
joint pain.
Enter CNS, damage blood vessels as well as brain
tissue.
Symptoms- above malaise, then change in personality
or behavior, decreased ability to concentrate, walk,
talk. Extreme tiredness during the day, insomnia at
night. Eventually coma, then death.
Easier drug treatment before CNS is involved, afterward,
highly toxic arsenic based drug.
Antigenic shifting of protozoan makes a vaccine
extremely difficult.
Controlling tse tse flies is best option in decreasing the
disease
Protozoan Diseases of the
Nervous System
• Primary Amebic Meningoencephalopathy
– Signs and symptoms
• Same as those of meningitis and encephalitis caused by
other microbes
– Pathogen, pathogenesis, and epidemiology
• Caused by Acanthamoeba and Naegleria
• Enter host through abrasions on the skin or the eyelid or
by inhalation of contaminated water
– Diagnosis, treatment, and prevention
• Drugs have limited success
• Prevented by avoiding possibly contaminated water
supplies
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Infectious Diseases Affecting the Nervous System.
Fig. 19.p608