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50 Cards in this Set

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Meningococcal Meningitis
Symptoms
– First symptoms similar regardless of agent
• Mild cold followed by onset of throbbing headache • Fever • Pain and stiffness of neck and back • Nausea and vomiting
• Deafness and alteration in consciousness may appear progressing to coma
Meningococcal Meningitis
Causative Agent
– Neisseria meningitis
• Gram-negative diplococci
• 12 antigenic serotypes
- Most serioues infections due to types A, B, C, and Y
Meningococcal Meningitis
Pathogenesis
– Acquired by inhaling infected respiratory droplets
– Bacteria adhere to mucous membranes via pili and multiply
– Invade bloodstream by passing through respiratory epithelium
• Bloodstream carries organisms to CSF
– Organisms phagocytized by PMNs
• Enter fluid in large numbers
– Inflammation causes swelling and infarcts to brain tissue
• Can also cause obstruction of outflow of CSF
– Causes brain to squeeze against skull
– Release of endotoxin causes drop in blood pressure leading to shock
Meningococcal Meningitis
Epidemiology
– N. meningitis more prone to cause epidemics
• Reasons unknown
– Can spread rapidly in
due to types A,B,C and Y
crowded stressed places
– Human only source of infection
– Transmission can occur with disease or asymptomatic carrier
• Organism recovered from 5% - 15% of healthy individuals
Meningococcal Meningitis
• The decline in meningitis due to H.influenzae has resulted in a marked overall decrease in bacterial meningitis and a shift in the peak incidence in older age groups
• Streptococcus pneumoniae is the leading cause of meningitis in adults
Listeriosis
Symptoms
– Most cases asymptomatic
– Symptoms include • Fever and muscle aches
• Sometimes nausea and diarrhea
• 75% of cases coming to medical attention have meningitis
– With typical symptoms of meningitis
Listeriosis
Causative Agent
– Listeria monocytogenes • Motile, non-spore forming, facultative anaerobe, Gram (+)
rod
Listeriosis
Pathogenesis
– Mode of entry usually obscure • Generally thought to enter through GI tract
– Bacteria penetrate intestinal mucosa then enter the bloodstream
• Leads to bacteremia
– Organism can cross the placenta
• Produces abscesses in fetal tissues
• Babies usually develop meningitis after 1-4 week incubation period
Listeriosis
Epidemiology
– Widespread in natural waters and vegetation
– Can be carried asymptomatically in animals and
humans
– Occurs on all continents except Antarctica
– Pregnant women, elderly and immuncompromised at highest risk
• Advised to refrain from soft cheeses and reheat leftovers – Epidemics have resulted from contaminated foods
• Organism can survive in commercially prepared foods and at refrigeration temperatures
Hansen's Disease (leprosy)
Symptoms
– Begins gradually
• Usually with onset of increased or decreased sensation in certain areas of skin
• These areas usually have changes in pigmentation
– Affected areas later enlarge and thicken
– Loss of hair, ability to sweat and sensation
– Nerves in extremities visibly enlarge – Changes most obvious in face
Hansen's Disease (leprosy)
Causative agent
– Mycobacterium leprae • Aerobic, acid-fast, rod shaped
– Grows slowly • Generation time approximately 12 days
Hansen's Disease (leprosy)
Pathogenesis
– Earliest detectable findings in humans is infection of small nerves of skin
– Only know human pathogen to preferentially attack peripheral nerves
– Grows slowly within macrophages
– Disease may spontaneously stop progressing – Tuberculoid leprosy
» Rarely transmitted to others – Uncommon form termed lepromatous leprosy
• High numbers of bacteria in mucous membranes with very little inflammation
Hansen's Disease (leprosy)
Epidemiology
– Transmission via direct
human-to-human contact
• Disease develops in small number of people
– Controlled by body defenses
– Natural infections occur in wild nine banded armadillos and mangabey monkeys
• Armadillos not a source of human infection
Hansen's Disease (leprosy)
Prevention and Treatment
– No proven vaccine
– Dapsone and rifampin used to arrest tuberculoid leprosy
• Treated for 6 months • Lepromatous treated for 2
years
– Combination therapy required to control resistance
Botulism
Symptoms
– Begins 12 to 36 hours post ingestion of
contaminated foods
– Begins with dizziness, dry mouth and blurred vision
– Abdominal symptoms include pain, nausea, vomiting and diarrhea or constipation
– Progressive paralysis ensues • Paralysis of respiratory muscles most common
cause of death
• Paralysis distinguishes botulism from other forms of food poisoning
Botulism
Causative Agent
Clostridium botulinum
• Gram (+), spore forming rod
shaped
– Endospores generally resist boiling for hours
• Killed by autoclaving – Produces toxin
• 7 different toxins – A, B, C1, D, E, F, G
» All produced by different strains
– A, B, E, F responsible for most human cases
Botulism
Pathogenesis
– Spores germinate in favorable environment
• Bacterial growth results in toxin release – Toxin resists digestion and is absorbed by small intestine – Toxin can circulate in blood stream for 3 weeks or more
– Toxin is neurotoxin • Acts against nervous system
• One of most powerful poisons known • Toxin attaches to motor nerves blocking function of
neurotransmitter – Causes paralysis
– Toxin is AB toxin • B portion binds and A portion enters nerve cell
Botulism
Prevention and Treatment
– Prevention depends on proper sterilization and sealing of canned food
– Heating food to 100°C for 15 minutes just prior to eating generally makes food safe to eat
• Can’t rely on smell, taste or appearance to detect contamination
– Treated by intravenous administration of antitoxin ASAP
• Antitoxin only neutralizes circulating toxin • Affected nerves recover slowly
– Gastric washing and surgical removal of tissues removes unabsorbed toxin
– Artificial respiration may be required for prolonged periods
Viral Meningitis
Symptoms
– Typically abrupt in onset
– Characterized by • Fever
• Severe headache above or behind eyes • Stiff neck with increased pain on forward flexion • Sensitivity to light • Nausea and vomiting
• May have sore throat, chest pain, swollen glands and skin rash
– Depends on causative agent
Viral Meningitis
Causative Agent
VViral Meningitis
• Symptoms
– Typically abrupt in onset
– Characterized by • Fever
• Severe headache above or behind eyes • Stiff neck with increased pain on forward flexion • Sensitivity to light • Nausea and vomiting
• May have sore throat, chest pain, swollen glands and skin rash
– Depends on causative agent
• Causative agent – Small, non-enveloped
RNA virus
– Member of the enterovirus subgroup of picornavirus family
– Responsible for at least half of viral meningitis cases
• Most common offenders are Coxsackie virus and Echovirus
Viral Meningitis
Pathogenesis
– Begins with infection of throat and intestinal epithelium
• Progresses to lymphoid tissue in the bloodstream
– Viremia results in meningeal infection
• May also be responsible for rash and chest pain
Viral Meningitis
Epidemiology
Enteroviruses transmitted by the fecal-oral route, mumps by respiratory secretions and saliva. Enteroviruses transmission mainly summer and early fall; mumps in fall an d winter.
Viral Meningitis
Prevention and Treatment
Handwashing, avoiding crowded swimming pools during enterovirus epidemics; mumps vaccine for mumps prevention. No specific treatment.
Viral Encephalitis
Symptoms
• Symptoms
– Onset usually abrupt
– Characterized by
• Fever
• Headache
• Vomiting
• One or more nervous system abnormalities
– Disorientation, localized paralysis, deafness, seizures or coma
Viral Encephalitis
Causative Agent
West Nile Virus
– Arboviruses • Arthropod borne viruses
– Transmitted by insects, mites and ticks
– Viruses enveloped single-stranded RNA viruses
Viral Encephalitis
Pathogenesis
• Pathogenesis
– Knowledge of pathogenesis incomplete – Viruses multiply at site of bite and in local lymph nodes
• Produces viremia – Virus crosses blood-brain barrier
• Mechanism unknown – Progression of disease halted with appearance of
neutralizing antibody – Mortality ranges from 2% to 50% depending on agent
Viral Encephalitis
Epidemiology
– Only minority infected develop encephalitis • Other develop viral meningitis
– Disease are all zoonoses • Maintained naturally in birds and rodents
– Humans are accidental hosts – LaCrosse encephalitis usually causes most cases of encephalitis
Infantile Paralysis (Polio)
Epidemiology
– Virus widespread in areas where sanitation is poor
• Virus usually spread via fecal-oral route
– In endemic areas people generally do not escape childhood without contracting disease
– Babies receive antibodies transplacental
• Babies develop disease within 2 to 3 months of age
– Develop lifelong immunity
Infantile Paralysis (Polio)
Prevention and Treatment
– Virus stable under natural conditions
– Control directed at vaccination
Infantile Paralysis (Polio)
Pathogenesis
- Infects throat and intestine
- Circulates via bloodstream
- Enters some motor nerve cells of brain or spinal cord
- Infected nerve cells lyse upon release of mature virus
Infantile Paralysis (Polio)
Epidemiology
Spreads by fecal-oral route; asymptomatic and nonparalytic cases common
Infantile Paralysis (Polio)
Prevention and treatment
Injected Salk's inactivated disease or Sabin's orally administered attenuated vaccine

Treatment: artificial ventiliation for respiratory paralysis; physical therapy and rehabilitation
Rabies
Symptoms
– Fever/Fatigue – Head and muscle ache – Sore throat – Nausea
– Tingling/twitching at site of viral entry
– Early symptoms begin 1 to 2 months post infection • Progress rapidly to secondary symptoms of
– Encephalitis, agitation, confusion, hallucinations, seizure, increased sensitivity to light and touch
• Body temperature rises with increased salivation and difficulty swallowing
– Results in frothing of mouth • Hydrophobia occurs in 50% of cases
• Coma develops • About 50% of patients die within 4 days after onset
Rabies
Causative Agent
– Rabies virus • Member of rhabdovirus family • Sticking bullet shape • Enveloped, single-stranded RNA genome
Rabies
Pathogenesis
– Mode of transmission primarily via saliva of rabid animal • Usually due to bite or abrasion • Can be contacted via inhalation
– Virus multiples in muscle cells at site of infection
– Virus reaches brain via infected nerve • Virus multiplies extensively in brain • Negri bodies form at sites of replication
Rabies
Epidemiology
Widespread in wild animals
• 5,000 cases reported annually in United States
– Skunks, raccoons and bats considered chief reservoir • Raccoons most infected • Almost all human cases due to contact with infected bats
– Zero to 4 reported cases in U.S annually • Only 25% have history of dog bite • Long incubation period of virus make history unreliable
Rabies
Prevention and Treatment
– Wash wound immediately and thoroughly • Use soap and water and apply antiseptic
– Risk of developing rabies from bite of rabid dog is approximately 30%
• Risk can be lowered considerably if vaccine is administered as soon as possible after exposure
– Presumably vaccine provokes better immune response
– Bitten individual should receive series of 5 injections at wound site and intramuscularly
• Shots should be given even if biting animal presumed to be rabid
– No effective treatment for rabies • Only six known survivors of disease
Cryptococcal Meningioencephalitis
Symptoms
• Symptoms
– Develop gradually in healthy individuals
– Generally consist of • Difficulty thinking • Dizziness • Intermittent headache • Slight or no fever
– Slow progression of disease results in other symptoms
• Vomiting • Weight loss • Paralysis • Seizures • Coma
Cryptococcal Meningioencephalitis
Causative Agent
– Yeast form of Filobasidiella neoformans fungus
– Small, spherical yeast
– Generally surrounded by large capsule
Cryptococcal Meningioencephalitis
Pathogenesis
– Fungus becomes airborne in dust • Enters body via inhalation and establishes infection first in
lung – Infection often eliminated by body defenses
– Organism multiplies and enters bloodstream – Capsule inhibits phagocytosis and neutralizes
opsonins
– Organisms typically cause thickening of meninges • This can often impede the flow of CSF • Also invade brain tissue producing abscesses
Cryptococcal Meningioencephalitis
Epidemiology
– Distributed worldwide in soil and vegetation • Numerous in soil where pigeon droppings
accumulate
– For every one case of disease millions are infected with organism
– Symptomatic infection often the first indicator of AIDS
– Person-to-person spread does not occur
African Sleeping Sickness
Symptoms
– First symptoms appear within a week after bite from tsetse fly
• Nodule develops at site of bite • Regional lymph nodes enlarge
– Symptoms may disappear spontaneously
– Weeks or years later recurrent fevers develop
– CNS involvement marked by gradual loss of interest in everything
• Marked by decreased activity and indifference to food – Eyelids droop and individual falls asleep during
everyday tasks – Speech becomes slurred followed by coma and death
African Sleeping Sickness
Causative Agent
– Trypanosoma brucei • Flagellated protozoan
• Slender with wavy undulating membrane
• Two subspecies – T. brucei rhodesiense
» Occurs mainly in cattle-raising areas of East Africa
– T. brucei gambiense
» Occurs mainly in forested areas of Central and West Africa
• Transmitted by tsetse fly
African Sleeping Sickness
Pathogenesis
– Protozoan enters through bite in fly saliva
– Organism multiplies at skin and migrates to lymphatic and blood circulation
• Body responds with fever and IgM antibody – Symptoms improve
– Period followed by recurrent increases in numbers of parasite
• Termed parasitemica – Parasitemia and antibody production continue until treatment or
death
– T. brucei rhodesiense infections progress quickly often with major system involvement with 6 weeks and death in 6 months
– T. brucei gambiense infections progress much more slowly
African Sleeping Sickness
Epidemiology
– Disease occurs on African continent within 15° of equator
– 10,000 to 20,000 new cases annually – Occurrence of disease is determined by
distribution of tsetse fly
– Wild animals main reservoir for Rhodesian form
– Humans are main reservoir for Gambian form • Human-to-human transmission more common
Transmissible Spongiform Encephalopathies
Symptoms
– Early symptoms • Vague behavioral changes • Anxiety • Insomnia • Fatigue
– These symptoms progress weeks to months to hallmark symptoms
• Muscle jerks • Lack of coordination • Dementia • Deteriorating intellectual function • Impaired judgment • Memory loss
– Disease often progresses to death within a year
Transmissible Spongiform Encephalopathies
Causative agent
– Proteinaceous infectious particles • a.k.a prions
• Appear to be new class of infectious agent – Differ from bacteria, viruses and viroids
– Main characteristics • Increase in quantity during incubation period
• Resist inactivation via UV and ionizing radiation • Resist inactivation by formaldehyde and heat • Not readily destroyed by proteases • Not destroyed by nucleases
• Much smaller than smallest virus • Composed of protein coded by normal cellular gene
– Modified after transcription
– Apparently arose following gene encoding normal prion protein
– Mutation caused protein to have different folding properties
– Mutated protein resistant to proteases
• Normal protein sensitive – Resists UV light and nucleases
• Due to lack of nucleic acid
– Inactivated by chemicals that denature proteins
Transmissible Spongiform Encephalopathies
Epidemiology
– Creutzfeld-Jakob occurs in humans over age 45
• Human-to-human transmission has occurred via corneal transplants
– Scrapie found in sheep • Most likely transmitted from ewe to lamb
– Mad cow disease result of cattle exposed to scrapie in cattle feed
– New varient Creutzfeld-Jakob mostly likely due to exposure of human to mad cow disease
• Median age of onset of NVCJ is 28 years
Transmissible Spongiform Encephalopathies
Prevention and Treatment
– Prions inactivated by
autoclaving in 1N NaOH
– No treatment • All forms are fatal
Transmissible Spongiform Encephalopathies
Pathogenesis
– No inflammatory or immune response produced
– Replication depends on presence of normal cellular protein
• Replicate by converting normal protein into copies of themselves
– Normal course of infections • Replication in spleen
– Most likely in dendritic cells
• Then transported to nervous system via nerve axon
• Prions aggregate in insoluble masses in nerve cells – Causes malfunction and death