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50 Cards in this Set
- Front
- Back
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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 |
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Meningococcal Meningitis
Causative Agent |
– Neisseria meningitis
• Gram-negative diplococci • 12 antigenic serotypes - Most serioues infections due to types A, B, C, and Y |
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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 |
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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 |
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Meningococcal Meningitis
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• 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 |
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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 |
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Listeriosis
Causative Agent |
– Listeria monocytogenes • Motile, non-spore forming, facultative anaerobe, Gram (+)
rod |
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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 |
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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 |
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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 |
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Hansen's Disease (leprosy)
Causative agent |
– Mycobacterium leprae • Aerobic, acid-fast, rod shaped
– Grows slowly • Generation time approximately 12 days |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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.
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Viral Meningitis
Prevention and Treatment |
Handwashing, avoiding crowded swimming pools during enterovirus epidemics; mumps vaccine for mumps prevention. No specific treatment.
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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 |
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Viral Encephalitis
Causative Agent |
West Nile Virus
– Arboviruses • Arthropod borne viruses – Transmitted by insects, mites and ticks – Viruses enveloped single-stranded RNA viruses |
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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 |
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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 |
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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 |
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Infantile Paralysis (Polio)
Prevention and Treatment |
– Virus stable under natural conditions
– Control directed at vaccination |
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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 |
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Infantile Paralysis (Polio)
Epidemiology |
Spreads by fecal-oral route; asymptomatic and nonparalytic cases common
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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 |
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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 |
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Rabies
Causative Agent |
– Rabies virus • Member of rhabdovirus family • Sticking bullet shape • Enveloped, single-stranded RNA genome
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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 |
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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 |
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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 |
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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 |
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Cryptococcal Meningioencephalitis
Causative Agent |
– Yeast form of Filobasidiella neoformans fungus
– Small, spherical yeast – Generally surrounded by large capsule |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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Transmissible Spongiform Encephalopathies
Prevention and Treatment |
– Prions inactivated by
autoclaving in 1N NaOH – No treatment • All forms are fatal |
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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 |
