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96 Cards in this Set

  • Front
  • Back
central nervous system infections (CNSI)
threatens persons ability to move feel and think normally
destroy nerve cells leaving victim paralyzed
complete loss of finger or toes and deformities
central nervous system
brain
skull
meninges
spinal cord
vertebrae
meningitis
inflamm or infection of meninges
bacterial meningitis
viral meningitis
meningoencephalitis
inflamm or infection of the meninges and the brain
high fever
headache
stiff neck, naausea and vomiting
photophobia
confusion, sleepiness, seizures
main causes of bacterial meningitis
strepto pneumoniae
neisseria meningitis
myvobacterium leprae
main causes of bacterial meningitis newborns
e coli k1
stepto agalactiae
listeria monocytogenes
bacterial meningitis
Inflammation of the covering of the brain and spinal column
Can result in irreversible neurological damage (blindness, deafness, learning deficiencies) and death
Spread by direct close contact with the discharges from the nose or throat of an infected person (crowded places like dorms, barracks, etc.)
bacterial meningitis symptoms
Persons over age 2 - high fever, headache, and stiff neck
Newborns and infants - symptoms of fever, headache, and neck stiffness may be hard to detect. Other signs in babies might be inactivity, irritability, vomiting, and poor feeding.
As the disease progresses, patients of any age can have seizures
bacterial meningitis prevention
depends on use of vaccines, rapid diagnosis, and prompt treatment of close personal contacts
There are vaccines against H. influenzae type B, some strains of N. meningitidis, and many types of S. pneumoniae
bacterial meningitis in newborns
Streptococcus agalactiae
Colonizes the vagina in 15-40% of pregnant women
A major cause of meningitis in newborns
Culture positive women treated with antibiotics prior to and during labor
Has led to a drop of > 75%
E. coli (Gram negative rods from mother’s GI tract)
Maternal antibodies against these are of the IgM type and thus do not cross the placenta
meningococcal meningitis symptoms
Cold, headache, fever, pain and stiffness of the neck and back, nausea and vomiting
progress to death w/n hours

Petechiae (purplish spots) appear on the skin
meningococcal meningitis
There are 13 antigenic groups of N. meningitidis, most serious infection are due to A, B, C, Y and W135
The causative agent of meningococcal meningitis is Neisseria meningitidis
meningoccal meningitis patho
Infection is acquired by inhaling airborne droplets from the respiratory tract of another person. Also, humans are the only source of the infection A). N. meningitidis attach to the mucous membrane by pili. B). They invade the bloodstram. C). The blood carries the bacteria to the meninges and cerebrospinal fluid
meningococcal meningitis treatment
A vaccine composed of purified capsular polysaccharides of N. meningitidis serogroup A, C, Y and W135 is availible The antibiotic rifampin is given as a prophylactic treatment to the people, who are intimately exposed to cases of meningococcal disease
spreads rapidly in overcrowded stressed populations
listeria monocytogenes
Motile, non-spore forming, facultative anaerobic Gram+ rod. Grows in macrophages and at 4oC
listeria monocytogenes patho
Worlwide distribution in animals, plants and soil

Transferred to humans by contact with animals or their feces, by unpasteurized milk and cheese, and by contaminated vegetables (Slaw)

Infections occur in primarily 2 clinical settings:
Fetus or newborn as a result of transmission across the placenta or during delivery
Infected mother may be asymptomatic or has an influenza-like illness

Immune suppressed patients
Can lead to sepsis or meningitis
listeria monocytogenes treatment
Cook meat thoroughly, wash row vegetables, avoid soft cheeses (when pregnant)
Ampicillin is an effective antibiotic against L. monocytogenes
hansens disease leprosy
is a granulomatous disease of the peripheral nervous system caused by Mycobacterium leprae
M. Leprae is aeroboc, acid-fast, and rod-shaped bacterium, which grows very slowly (generation time: ~ 12 days
hansens disease leprosy symptoms
Onset of increased or decreased sensation in certain areas of skin, which later enlarge and thicken.

The nervous system of the arms and legs becomes visibly enlarged with accompanying pain, later changing to numbness, muscle wasting, ulceration, and loss of fingers or toes.
tuberculoid leprosy
is the limited type of leprosy disease in which cellular immunity suppresses proliferation of the M. leprae
lepromatous leprosy
When cellular immunity and delayed hypersensitivity to M. leprae fail to develop or are suppressed, unrestricted growth of M. leprae occours in the skin macrophages and peripheral nerves,- this form of Hansen’s disease
lepromatous leprosy epid
direct human-to-human contact. The source of the organisms is mainly nasal secretions of a lepromatous case.
Natural infections with M. leprae occur in wild nine-banded armadillos and in mangabey monkeys
lepromatous leprosy treatment
Dapsone, rifampin, and clofazimine are effective antibiotics against M. leprae
No vaccine against leprosy is yet availible
botulism
principal symptom is paralysis
Clostridium botulinum
Gram (+), spore forming rod
Endospores generally resist boiling for hours
Killed by autoclaving
three types foodborne, intestinal and wound
botulism epid
produces endospores that are highly resistant. The spores germinate if the environment is favorable and growth of the bacteria results in the release of exotoxin into the food. The exotoxin can be absorbed by the small intestine, and can circulate in the blood-stream for several weeks. This toxin is a neurotoxin, and is one of the most powerful toxins known.
botulism symptoms
Dizziness, dry mouth, blurred or double vision, abdominal pain or diarrhea. But most dangerous form is paralysis
botulism epid
is widely distributed in soils and aquatic sediments around the world. In the early part of the twentieth century, outbreaks of foodborne botulism were common in the United States. Today, intestinal botulism is much more common.
botulism treatment
The toxin is heat-labile, and heating food to 100°C for 15 min. just prior to serving generally makes it safe to eat.
Cleaning infected wounds of dirt and dead tissue.
Intravenous administration of antitoxin.
viral meningitis
Aseptic meningitis
Meningitis not due to a bacterial pathogen

Viral meningitis is much more common than bacterial meningitis, but it is usually a mild diseaseSmall, non-enveloped RNA virus, member of the enterovirus subgroup of picornaviruses, are responsible for at least half of viral meningitis cases.
Most common offenders are coxsackie viruses (cause throat or chest pain) and
echo viruses (cause rash)
Mumps an infrequent cause
viral meningitis symptoms
Typically abrupt in onset
Similar to bacterial meningitis (headache, pain, nausea and vomiting)
Usually a benign illness
viral meningitis patho
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 epid
Relatively stable in environment
Can survive in chlorinated water
Infected often eliminate virus in feces
Often for weeks
Transmission via fecal-oral route
Mumps virus transmitted via respiratory droplets
viral meningitis treatment
Handwashing and avoidance of crowded swimming pools
When aseptic disease present in community
No vaccine against coxsakievirus and echoviruses
Mumps virus controlled via immunization
viral encephalitis
can cause permanent disability or death
Arboviruses
Arthropod borne viruses
Togavirus (Eastern and Western Equine Viruses)
Flavivirus (St. Louis encephalitis, yellow fever, dengue virus)
Bunyavirus (California equine virus)
Reovirus (Colorado tick fever virus)
Transmitted by insects, mites and ticks
Viruses enveloped single stranded RNA viruses
viral encephalitis symptoms
Onset usually abrupt
Fever, headache, vomiting, and one or more CNS abnormalities
Disorientation, localized paralysis, deafness, seizures or coma
viral encephalitis patho
Viruses multiply at site of bite and in local lymph
nodes
Produces viremia
Virus crosses blood-brain barrier
Causes extensive damage to brain tissue in severe
cases
Progression of disease halted with appearance of neutralizing antibody
Mortality ranges from 2% to 50% depending of type of infecting agent
Disabilities often present in those who recover
viral encephalitis treatment
Animals often used to identify emergence of disease
Prevention directed towards
Avoiding outdoor activities at night when mosquito populations highest
Make sure windows and porches properly screened
Use insect repellents and insecticides
No proven antiviral therapy
poliomyelitis
Causative agent- Poliovirus
Picornavirus (non-enveloped, single stranded RNA viruses)
3 antigenic types
Protection requires antibody to all 3 types
Characteristic feature of poliomyelitis is selective destruction of motor nerve cells
poliomyelitis patho
Transmission occurs by the fecal-oral route
Immune system conquers infection in most people
Viruses spreads through blood stream to CNS
Virus replicates in motor nerves of the brain and spinal cord
poliomyelitis symptoms
Headache, fever, stiff neck, nausea, pain, paralysis, muscle-shrinking and in an infected area the bones do not develop normally
poliomyelitis treatment
Babies receive antibodies transplancentally from their mothers
Control directed at vaccination
Salk vaccine
Inactivated vaccine (formalin-killed)
Sabin vaccine
Attenuated vaccine
Advantages
Given orally
Induces sec. IgA which interrupts fecal-oral transmission
Disadvantages
Rare reversions
Can cause disease in Immune deficient individuals
Infection of other enteroviruses in GI tract can limit replication of vaccine virus and limit protection
Must be refrigerated.
rabies
Causative agent- rabies virus
Rhabdovirus family (enveloped, single stranded RNA viruses)
most feared of all diseases because of its terrifying symptoms
rabies symptoms
Fever, headache, nausea, vomiting, sore throat; later, spasms of the muscles of mouth and throat, coma.
rabies patho
Transmission of rabies to humans occurs via the saliva of a rabid animal
When the virus enters an axon it is carried along the course of the nerve by the normal flow of the axon’s cytoplasm, eventually reaching the brain. The virus then multiplies extensively in brain tissue, causing the symptoms of encephalitis. Characteristic inclusion bodies, formed by rabies virus, are called Negri bodies
rabies epid
Bite of rabid animal, usually a bat, and/or inhalation
raibes treatment
Avoid suspect animals. Immunize pets, immedietly wash wound and apply antiseptic
cryptococcal meningoencephalitis
Cryptococcal meningitis is an infection of the meninges and brain by fungus Cryptococcus neoformans
crpto menin syptoms
dizziness, headache, vomiting, weight loss, seizure, paralysis, and coma
crpto menin patho
Infection starts in lung. C. neoformans multiply, enter the bloodstream and are carried to various parts of the body. They can invade the meninges and the brain.
crypto menin epid
C. neoformans is located in soil and vegetation, especially in soil where pigeon droppings accumulate. Infection is contracted by inhaling contaminated dust
crypto menin treatment
No vaccine or other preventive measure available. Treatment with the antibiotic amphotericin B is effective
african trypanosomiasis
Trypanosomiasis is an Infection of the blood and central nervous system caused by trypanosoma
african trypanosomiasis symptoms
fever, headache, uncontrollable sleepiness, poor concentration, and coma
african trpy patho
During the bite by an infected tsetse fly, the trypanosomes enter the bite wound in the fly’s saliva. Trypanosomes multiply and enter the lymphatic and blood circulation. They can infect the CNS
african tryp epid
African trypanosomiasis occurs on the African continent with 10.000 - 20.000 new cases each year. The occurrence of the disease is determined by the distribution of the tsetse fly vectors.
african tryp treatment
Protective clothing, insecticides; Melarsporol, eflornithine, and suramin
transmissible spongiform
Encephalopathy (TSE)
TSE is a brain disease. It is very rare in humans (1/1.000.000 people
Prions (PrP)
proteinaceous infectious particles
tse symptoms
Muscle jerks, lack of coordination, memory loss, and loss of muscle function
tse patho
Infection starts in the spleen and other lymphoid tissues. The prions are then transported to the central nervous system by B lymphocytes.
tse epid
Generally occurs in individuals older than 45 years. Transmission of cattle prions to humans probably occurred by eating contaminated beef.
tse treatment
Using of absolutely sterile surgical instruments. Autoclaving inactivate prions
gram negative septicema
Gram (-) bacteria more likely cause of fatal septicemia
Shock is common despite treatment
Mortality rate nearly 50%
Blood cultures from patients usually reveal
E. coli
Gram (-) facultative anaerobe
P. aeruginosa
Gram (-) aerobe
Generally found in natural environment
Bacteroides sp.
Gram (-) aerobe
Part of normal intestinal and upper respiratory flora
gn septicemia symptoms
Chills, fever, low-blood pressure
tularemia rabbit fever
F. tularensis
High virulent (Category A agent of biological terrorism), Non-motile, aerobic Gram (-) rod. It requires a special medium enriched with cysteine in order to grow.
serious infectious disease
rabbit fever patho
F. tularensis causes ulcer where it enters the skin.
It spreads via lymphatic and
blood vessels.
Pneumonia occurs when bacteria infect the lung from the bloodstream or by inhalation.

F. tularensis can survive and replicate in macrophages.

Syndromes: Ulceroglandular (70-85%), glandular, typhoidal, pneumonic, oculoglandular, oropharyngeal
rabbit fever symptoms
Ulcer in side of entry, enlarged lymph nodes, fever, chills, and achiness.
rabbit fever epid
In the west US infections result from the bites of infected ticks
and deer flies, and usually occur during the summertime.

In Europe epidemics of inhalation tularemia have occurred from
dust arising from moving lawns or rodent infested buildings.
skinning rabbits
rabbit fever treatment
Uses of Rubber gloves and goggles when working with animal carcasses
Inspect routinely for ticks after exposure
Live, attenuated vaccine available for workers at higher risk of exposure
Streptomycin is DOC but also treated with gentimicin
cell mediated imunity
francisella tularenis
95% DNA genomic sequence identity
tularensis (type A)
holarctica (type B)
novicida
tularensis type a
Two copies of FPI (Francisella Pathogenicity Island)
highly virulent in humans
potential bioweapon (CDC)
holarctica type b
Two copies of FPI
moderately virulent in humans
live vaccine strain (LVS) is an attenuated form of holarctica
novicida
One copy of FPI (97% homology to spp. tularensis)
avirulent to humans, unless immunocompromised
virulent to mice
brucellosis undulant fever
Four varieties of genus Brucella cause disease in humans (all fall into a single species Brucella melitensis)
Traditionally each variety given own species name depending on preferred host
B. abortus -cattle
B. canis - dogs
B. melitensis - goats
B. suis - pigs
Organism is Gram (-) rod
domestic animals
undulant fever symptoms
Onset usually gradual and symptoms are vague
Aches and pains, enlarged lymph nodes, weight loss, and fever
Because of the recurrence in some cases of fevers over weeks or months, brucellosis is also called: “undulant fever”.
Without treatment most cases recover within 2 months
15% will be symptomatic for 3 months or longer
undulant fever epid
Chronic infection of domestic animals
Generally involving the mammary gland and uterus (organs rich in sugar)
Causes contaminated milk and abortions
Abortion not a feature of human disease
Occurs in workers in meat packing industry
Major problem in animals used for food
undulant fever patho
Organism penetrates mucous membranes or break in skin
Disseminated via lymphatic or blood vessels
Generally to heart and kidneys
Spleen enlarges in response to infection
Organisms resistant to phagocytic killing
Can grow within phagocytes
(inaccessible to antibodies or antibiotics)
Mortality generally due to endocarditis
The most frequent serious complication is bone infection, Osteomyelitis
undulant fever treatment
Pasteurization most important control measure
- Inspection of domestic animals
- Protective eyewear and gloves when working with animals or animal carcass
- Attenuated vaccine controls disease in domestic animals
- Tetracycline combined with rifampin used for treatment
Treatment usually given for 6 weeks (very slow growing organisms)
plaugue black death
Plague, once known as the “black death” is caused by Yersinia pestis
Yersinia pestis is a facultative intracellular bacterium, which grows best at 28ºC.
plague black death symptoms
Develop abruptly 1 – 6 days post infection
Transmission via bite from infected flea
Disease characterized by large tender lymph nodes called buboes (hence the name Bubonic Plague)
Other symptoms include
High fever
Shock
Delirium
Patchy bleeding under the skin
May also have cough and bloody sputum
Only if lungs infected (Pneumonic plague)
The dark hemorrhages in the skin inspired the
name “black death”
black death patho
Masses of organism obstruct digestive tract of rat fleas
Flea regurgitates infected material into bite wound
Most organisms destroyed by neutrophils
Organisms multiply within macrophages
Produces capsule while in macrophages but not in fleas
Macrophages die and release organism. Organism encapsulated and produces Yop proteins and other mechanisms that enhance survival. Inflammation in lymph nodes results in swelling. Lymph nodes become necrotic and spill organisms into the bloodstream - Septicemic plague (endotoxin release results in shock and disseminated intravascuolar coagulation (DIC).
Infection of the lung results in pneumonic plaque
plague treatment
Prevention directed by rat control
Proper garbage disposal
Rat-proof buildings
Guards on mooring ropes
Extermination programs
Killed vaccine gives short-term partial protection
Treatment via tetracycline for some exposed individuals to control epidemics. Gentamycin, ciprofloxacin and doxycycline effective if given early
infectious mononucleosis
Mononucleosis is a viral infection that produces flu-like symptoms. Infected people have an increased number of mononuclear leukocytes in their blood
Epstein-Barr virus
Double stranded DNA virus
Belongs to herpesvirus family
EB virus was first isolated from Burkitt’s lymphoma, a malignant tumor derived from B lymphocytes
infectious mononucleosis symptoms
Appear after long incubation
Usually 30 to 60 days post infection
Symptoms include fever, sore throat covered with pus, fatigue, enlarged lymph nodes and spleen
Most cases fever and sore throat disappear within 2 weeks, lymph node enlargement within 3 weeks
Infection leads to increased number of mononuclear cells in blood stream
infectious mononucleosis patho
Virus infects certain cell types that express the receptor for complement C3D component (CR2 or CD21)
Epithelial cells of oro/naso-pharynx and B cells
Infection begins in cells of throat and mouth
Virus carried to lymph nodes after replication in epithelial cells of mouth, saliva producing glands and throat
Infects B lymphocytes
Infection can be productive or nonproductive
Productive – kills cells
Nonproductive – virus is latent
Virus activates B cells to produce multiple clones of B lymphocytes to proliferate and produce immunoglobulin
T lymphocytes destroy infected B cells. Abnormal-appearing lymphocytes are activated T cells
infectious mononucleosis epid
Distributed worldwide
Infects individuals in crowded, economically disadvantaged areas
Infects at early age without producing symptoms producing immunity
More affluent populations missed exposure and lack immunity
Occurs almost exclusively in adolescents and adults who lack antibody
Virus present in saliva for up to 18 months
Mouth-to-mouth kissing important mode of transmission
No animal reservoir
infectious mononucleosis treatment
Avoiding saliva of another person
Kissing, sharing soft drinks
No vaccine
Acyclovir inhibits productive infection
Has no activity on latent viruses
yellow fever
Enveloped, single stranded RNA arbovirus
Belongs to flavivirus family
Virus multiplies in mosquitoes
RNA arbovirus, that is transmitted to humans through the bite of infected mosquitoes
yellow fever patho
Mosquitoes (Aedes mosquitoes) transmit virus to humans via bite.
Multiplies and enters blood stream
Carried to liver
Jaundice results in liver damage
Injury to small blood vessels leading to DIC
Damage heart muscle
Kidney failure is a common consequence of disease
Loss of circulating blood and low blood pressure
yellow fever symptoms
Disease can range from mild to severe
Most common form may be fever and slight headache lasting a day or two
Severe disease: high fever, nose bleeds and bleeding into the skin, “black vomit” from GI bleeding and jaundice (hence the name “Yellow Fever”)
Mortality rate of severe disease can reach 50%
Reason for the variation in symptoms is unknown
yellow fever epid
Reservoir mainly infected mosquitoes and primates in tropical regions of Central and South America and Africa
Periodically spread to urban areas via mosquito bite
tellow fever treatment
Control achieved by spraying and elimination of breeding sites of its principal vector Aedes egypti (almost impossible in jungle regions)
Attenuated vaccine available for high risk groups
No proven antiviral treatment
malaria
Human malaria caused by four species of genus Plasmodium
P. vivax, P. falciparum, P. malatiae, P. ovale
Infectious form of parasite injected via Anopheles mosquito
malaria symptoms
First symptoms: fever, headache, and pain in the joints and muscles
After 2-3 weeks the symptoms fall into three phases highly suggestive of malaria
Cold phase
Hot phase
Wet phas
malaria patho
The characteristic feature of malaria (after high fever feeling healthy again), results from erythrocytic cycle of growth and release of merozoites
Mararia is the most common cause of splenic rupture, which can occur with, or without trauma
P. falciparum tends to be very severe. It infects erythrocytes of all ages
Other Plasmodium species infect only young or old erythrocytes
P. vivax and P. ovale develop treatment-resistant forms and, months after treatment, they can begin multiplying in exoerythrocytic cycle
malaria epid
Once common in both temperate and tropical areas
Now dominant disease of warm climate
Eliminated from continental U.S. in late 1940’s
Mosquitoes of genus Anopheles are biological vectors
Infected mosquitoes and humans constitute reservoir
Transmission via mosquitoes, blood transfusion and sharing of syringes
malaria treatment
Mosquito control
Treatment is complicated
Due to different stages of mosquito life cycle
Chloroquine
Effective against erythrocyte stage
Will not cure liver infection
Primaquine and tafenoquine
Generally effective against exoerythrocyte stage and certain species gametocytes