The Phobia List
There are many hundreds of named phobias, and this is the most complete list of which we know.
Although there are many hundreds of 'different' phobias, all phobias are in fact very similar: a particular stimulus, be it spiders, snakes, or pretty well anything else triggering the phobic individuals fear response when it isn't appropriate.
The Phobia List: A
Ablutophobia — Fear of washing, bathing, or cleaning
Acarophobia — Fear of itching or the insects that cause itching
Acerophobia — Fear of sourness or things that are sour
Achluophobia — Fear of darkness or the dark
Acousticophobia — Fear of noise or sound
Acrophobia — Fear of heights or high levels
Aeroacrophobia — Fear of open high places
Aeronausiphobia — Fear of vomiting secondary to airsickness
Aerophobia — Fear of draft, swallowing air, or airbourne noxious substances
Agateophobia — Fear of insanity or becoming insane
Agliophobia — Fear of pain
Agoraphobia — Fear of open spaces, leaving a safe place, or crowded public places
Agraphobia — Fear of sexual abuse
Agrizoophobia — Fear of wild animals
Agyrophobia — Fear of streets or crossing the street
Aichmophobia — Fear of needles, pins, or pointed objects
Ailurophobia — Fear of cats
Albuminurophobia — Fear of kidney disease
Alektorophobia — Fear of chickens
Algophobia — Fear of garlic
Alliumphobia — Fear of opinions or beliefs
Altophobia — Fear of dust
Amathophobia — Fear of riding in cars
Amaxophobia — Fear of walking
Amnesiphobia — Fear of amnesia
Amychophobia — Fear of scratches or being scratched
Anablephobia — Fear of looking up
Androphobia — Fear of men
Anemophobia — Fear of wind or air drafts
Anginophobia — Fear of angina, choking, or narrowness
Anglophobia — Fear of England, English Culture, or English People
Angrophobia — Fear of anger or becoming angry
Ankylophobia — Fear of immobility of a joint
Anthophobia — Fear of flowers
Anthropophobia — Fear of people or society
Antlophobia — Fear of floods
Anuptaphobia — Fear of staying single
Anxiety — Fear of Anxiety
Apeirophobia — Fear of infinity
Aphenphosmphobia — Fear of being touched
Apiphobia — Fear of bees
Apotemnophobia — Fear of persons with amputations
Arachibutyrophobia — Fear of peanut butter sticking to the roof of the mouth
Arachnephobia — Fear of spiders
Arithmophobia — Fear of numbers
Arsonphobia — Fear of fire or flames
Asthenophobia — Fear of fainting or weakness
Astraphobia — Fear of thunder and lightning
Astrophobia — Fear of stars and celestial space
Asymmetriphobia — Fear of asymmetrical things
Ataxiophobia — Fear of ataxia (muscular incoordination)
Ataxophobia — Fear of disorder or untidiness
Atelophobia — Fear of imperfection
Atephobia — Fear of ruin or ruins
Athazagoraphobia — Fear of being forgotton, being ignored, or forgetting
Atomosophobia — Fear of atomic explosions
Atychiphobia — Fear of failure
Aulophobia — Fear of flutes
Aurophobia — Fear of gold
Auroraphobia — Fear of Northern lights
Autodysomophobia — Fear of one that has a vile odor
Automatonophobia — Fear of ventriloquist's dummies, animatronic creatures or wax statues
Automysophobia — Fear of being dirty
Autophobia — Fear of solitude, being alone, oneself, or being by oneself
Aviophobia — Fear of flying
The Phobia List: B
Bacillophobia — Fear of microbes
Bacteriophobia — Fear of bacteria
Ballistophobia — Fear of missiles or bullets
Barophobia — Fear of gravity
Basiphobia — Fear of inability to stand or falling
Bathmophobia — Fear of stairs or steep slopes
Bathophobia — Fear of depth
Batophobia — Fear of heights or being close to high buildings
Batrachophobia — Fear of amphibians, frogs, newts, or salamanders
Bibliophobia — Fear of books
Blennophobia — Fear of slime
Body Dysmorphic Disorder — Fear of having ugly or unattractive features
Bogyphobia — Fear of bogies or the bogeyman
Bolshephobia — Fear of Bolsheviks
Botanophobia — Fear of plants
Bromidrophobia — Fear of bodily odor or bodily smell
Bufonophobia — Fear of toads
The Phobia List: C
Cacophobia — Fear of ugliness or things that are ugly
Cainophobia — Fear of newness or novelty
Caligynephobia — Fear of beautiful women
Cancerophobia — Fear of cancer
Cardiophobia — Fear of the heart
Carnophobia — Fear of meat
Catagelophobia — Fear of being ridiculed or ridicule
Catapedaphobia — Fear of jumping from high and low places
Cathisophobia — Fear of sitting
Catoptrophobia — Fear of mirrors
Cheimaphobia — Fear of cold
Chemophobia — Fear of chemicals or working with chemicals
Cherophobia — Fear of gaiety
Chionophobia — Fear of snow
Chirophobia — Fear of hands
Cholerophobia — Fear of anger or Cholera
Chorophobia — Fear of dancing
Chrematophobia — Fear of money
Chromatophobia — Fear of colors
Chronomentrophobia — Fear of clocks
Chronophobia — Fear of time
Claustrophobia — Fear of confined or small spaces
Cleisiophobia — Fear of being locked in an enclosed place
Cleithrophobia — Fear of being enclosed
Cleptophobia — Fear of stealing
Climacophobia — Fear of stairs, climbing stairs, or falling down stairs
Clinophobia — Fear of going to bed
Cnidophobia — Fear of stings or being stung
Coimetrophobia — Fear of cemeteries
Coitophobia — Fear of coitus, sex, or sexual intercourse
Cometophobia — Fear of comets
Coprastasophobia — Fear of constipation
Coprophobia — Fear of feces and fecal matter
Coulrophobia — Fear of clowns
Counterphobia — Fear of The preference by a phobic for fearful situations
Cremnophobia — Fear of precipices
Cryophobia — Fear of extreme cold, ice, or frost
Crystallophobia — Fear of crystals or glass
Cyberphobia — Fear of computers or working on a computer
Cyclophobia — Fear of bicycles
Cymophobia — Fear of waves or wave-like motion
Cynophobia — Fear of dogs, canines, or rabies
Cyprianophobia — Fear of prostitutes, venereal disease, or STDs
The Phobia List: D
Daemonophobia — Fear of demons or daemons
Decidophobia — Fear of making decisions
Defecaloesiophobia — Fear of painful bowels movements
Deipnophobia — Fear of dining or dinner conversation
Demophobia — Fear of crowds
Dendrophobia — Fear of trees
Dentophobia — Fear of dentists
Dermatopathophobia — Fear of skin disease or skin lesions
Dextrophobia — Fear of objects at the right side of the body
Diabetophobia — Fear of diabetes
Didaskaleinophobia — Fear of going to school
Dikephobia — Fear of justice
Dinophobia — Fear of dizziness or whirlpools
Diplophobia — Fear of double vision
Dipsophobia — Fear of drinking
Dishabiliophobia — Fear of undressing in front of someone
Doraphobia — Fear of fur or skins of animals
Doxophobia — Fear of expressing opinions or of receiving praise
Driving Phobia — Fear of driving a motorized vehicle
Dromophobia — Fear of crossing streets
Dutchphobia — Fear of the Netherlands, the Dutch, Dutch Culture
Dysmorphophobia — Fear of deformity
Dystychiphobia — Fear of accidents
The Phobia List: E
Earthquakophobia — Fear of earthquakes
Ecclesiophobia — Fear of churchs
Eisoptrophobia — Fear of mirrors or of seeing oneself in a mirror
Electrophobia — Fear of electricity
Eleutherophobia — Fear of freedom
Emetophobia — Fear of vomiting or throwing up
Enetophobia — Fear of pins
Enissophobia — Fear of having committed an unpardonable sin or criticism
Entomophobia — Fear of insects or bugs
Eosophobia — Fear of dawn or daylight
Ephebiphobia — Fear of teenagers
Epistaxiophobia — Fear of nosebleeds
Epistemophobia — Fear of knowledge
Equinophobia — Fear of horses
Eremophobia — Fear of being oneself or lonliness
Ereuthophobia — Fear of redlights, blushing, or the color red
Ergasiophobia — Fear of work, functioning, or Surgeon's operating
Ergophobia — Fear of work
Erotophobia — Fear of sexual love or sexual questions
Euphobia — Fear of hearing good news
The Phobia List: F
Francophobia — Fear of France, French people, or French culture
Frigophobia — Fear of cold or cold things
The Phobia List: G
Gamophobia — Fear of marriage
Geliophobia — Fear of laughter
Geniophobia — Fear of chins
Genuphobia — Fear of knees
Gephydrophobia — Fear of crossing bridges
Gerascophobia — Fear of growing old or old people
Germanophobia — Fear of Germany, German People, or German culture
Geumaphobia — Fear of taste
Globophobia — Fear of balloons
Glossophobia — Fear of speaking in public or trying to speak
Graphophobia — Fear of writing or handwriting
Gymnophobia — Fear of nudity
Gynephobia — Fear of women
The Phobia List: H
Hadephobia — Fear of hell
Hagiophobia — Fear of saints or holy things
Harpaxophobia — Fear of being robbed
Hedonophobia — Fear of feeling pleasure
Heliophobia — Fear of the sun
Hellenologophobia — Fear of Greek terms or complex scientific terminology
Helminthophobia — Fear of being infested with worms
Hemaphobia — Fear of blood
Hereiophobia — Fear of challenges to official doctrine or of radical deviation
Herpetophobia — Fear of reptiles or creepy, crawly things
Heterophobia — Fear of the opposite sex
Hierophobia — Fear of priests or sacred things
Hippopotomonstrosesquippedaliophobia — Fear of long words
Hobophobia — Fear of bums or beggars
Hodophobia — Fear of road travel
Homichlophobia — Fear of fog
Homilophobia — Fear of sermons
Homophobia — Fear of sameness, monotony, homosexuality, or becoming homosexual
Hoplophobia — Fear of firearms
Hormephobia — Fear of shock
Hyalophobia — Fear of glass
Hydrargyophobia — Fear of mercurial medicines
Hydrophobia — Fear of water
Hydrophobophobia — Fear of rabies
Hygrophobia — Fear of liquids, dampness, or moisture
Hylephobia — Fear of materialism or epilepsy
Hypegiaphobia — Fear of responsibility
Hypnophobia — Fear of sleep or being hypnotized
The Phobia List: I
Iatrophobia — Fear of doctors or going to the doctor
Ichthyophobia — Fear of fish
Ideophobia — Fear of ideas
Illyngophobia — Fear of vertigo or feeling dizzy when looking down
Insomnia — Fear of Inability to Sleep
Iophobia — Fear of poison
Isopterophobia — Fear of termites, insects that eat wood
The Phobia List: J
Japanophobia — Fear of Japanese
Judeophobia — Fear of Jewish People
The Phobia List: K
Kakorrhaphiophobia — Fear of failure or defeat
Kenophobia — Fear of voids or empty spaces
Kinesophobia — Fear of movement or motion
Koinoniphobia — Fear of rooms
Kolpophobia — Fear of genitals, particularly female
Kopophobia — Fear of fatigue
Kosmikophobia — Fear of cosmic phenomenon
Kyphophobia — Fear of stooping
The Phobia List: L
Lachanophobia — Fear of vegetables
Lalophobia — Fear of speaking
Lepraphobia — Fear of leprosy
Leukophobia — Fear of the color white
Levophobia — Fear of things to the left side of the body
Ligyrophobia — Fear of loud noises
Lilapsophobia — Fear of tornado or hurricanes
Limnophobia — Fear of lakes
Linonophobia — Fear of string
Liticaphobia — Fear of lawsuits
Lockiophobia — Fear of childbirth
Logizomechanophobia — Fear of computers
Logophobia — Fear of words
Luiphobia — Fear of lues or syphillis
Lutraphobia — Fear of otters
The Phobia List: M
Macrophobia — Fear of long waits
Mageirocophobia — Fear of cooking
Malaxophobia — Fear of love play
Maniaphobia — Fear of insanity
Mastigophobia — Fear of punishment
Mechanophobia — Fear of machines
Medomalacuphobia — Fear of losing an erection
Medorthophobia — Fear of an erect penis
Megalophobia — Fear of large things
Melanophobia — Fear of the color black
Melophobia — Fear of music
Meningitophobia — Fear of brain disease
Menophobia — Fear of menstruation
Merinthophobia — Fear of being bound or tied up
Metallophobia — Fear of metal
Metathesiophobia — Fear of changes
Meteorophobia — Fear of meteors
Metrophobia — Fear of poetry
Microbiophobia — Fear of microbes
Microphobia — Fear of small things
Misophobia — Fear of being contaminated with dirt or germs
Mnemophobia — Fear of memories
Monopathophobia — Fear of definite disease
Motorphobia — Fear of automobiles
Mottephobia — Fear of moths
Murophobia — Fear of mice
Mycophobia — Fear of mushrooms
Myrmecophobia — Fear of ants
Mythophobia — Fear of myths, stories, or false statements
The Phobia List: N
Narcissistic Personality Disorder — Fear of -
Necrophobia — Fear of death or dead things
Neopharmaphobia — Fear of new drugs
Nephophobia — Fear of clouds
Noctiphobia — Fear of the night
Nomatophobia — Fear of names
Nosocomephobia — Fear of hospitals
Nosophobia — Fear of becoming ill
Nostophobia — Fear of returning home
Novercaphobia — Fear of your step-mother
Nucleomituphobia — Fear of nuclear weapons
Nudophobia — Fear of nudity or nakedness
Nyctohylophobia — Fear of dark wooded areas or forests at night
The Phobia List: O
Obesophobia — Fear of gaining weight
Ochlophobia — Fear of crowds or mobs
Ochophobia — Fear of vehicles
Octophobia — Fear of the figure 8
Odontophobia — Fear of teeth or dental surgery
Oenophobia — Fear of wines
Oikophobia — Fear of houses, home surroundings, or being in a house
Olfactophobia — Fear of smells
Ombrophobia — Fear of rain or of being rained on
Ommatophobia — Fear of eyes
Oneirogmophobia — Fear of wet dreams
Oneirophobia — Fear of dreams
Onomatophobia — Fear of hearing a certain word or of names
Ophidiophobia — Fear of snakes
Ophthalmophobia — Fear of being stared at
Opiophobia — Fear of Fear of medical doctors experience of prescribing needed pain medications for patients
Optophobia — Fear of opening one's eyes
Ornithophobia — Fear of birds
Orthophobia — Fear of property
Ostraconophobia — Fear of shellfish
Ouranophobia — Fear of heaven
The Phobia List: P
Pagophobia — Fear of ice or frost
Panophobia — Fear of everything
Panthophobia — Fear of suffering or disease
Papaphobia — Fear of the Pope
Papyrophobia — Fear of paper
Paralipophobia — Fear of neglecting duty or neglecting responsibility
Paraphobia — Fear of sexual perversion
Parasitophobia — Fear of parasites
Paraskavedekatriaphobia — Fear of Friday the 13th
Parthenophobia — Fear of virgins or young girls
Pathophobia — Fear of disease
Patroiophobia — Fear of heredity
Peccatophobia — Fear of sinning
Pediculophobia — Fear of lice
Pediophobia — Fear of dolls
Pedophobia — Fear of children
Peladophobia — Fear of bald people
Pellagrophobia — Fear of pellagra
Peniaphobia — Fear of poverty
Pentheraphobia — Fear of mother-in-law
Phagophobia — Fear of swallowing or eating
Phalacrophobia — Fear of becoming bald
Pharmacophobia — Fear of taking medicine or drugs
Phengophobia — Fear of daylight or sunshine
Philemaphobia — Fear of kissing
Philophobia — Fear of falling in love or being in love
Philosophobia — Fear of philosophy
Phobophobia — Fear of phobias
Phonophobia — Fear of noises, voices, one's own voice, or telephones
Photoaugliaphobia — Fear of glaring lights
Photophobia — Fear of light
Phronemophobia — Fear of thinking
Phthisiophobia — Fear of tuberculosis
Placophobia — Fear of tombstones
Plutophobia — Fear of wealth
Pneumatiphobia — Fear of spirits
Pnigerophobia — Fear of choking of being smothered
Pogonophobia — Fear of beards
Poliosophobia — Fear of contracting poliomyelitis
Politicophobia — Fear of politicians
Polyphobia — Fear of many things
Ponophobia — Fear of overworking or of pain
Porphyrophobia — Fear of the color purple
Potamophobia — Fear of rivers or running water
Potophobia — Fear of alcohol
Proctophobia — Fear of rectums
Prosophobia — Fear of progress
Psellismophobia — Fear of stuttering
Psychophobia — Fear of the mind
Psychrophobia — Fear of the cold
Pteromerhanophobia — Fear of flying
Pteronophobia — Fear of being tickled by feathers
Pupaphobia — Fear of puppets
Pyrexiophobia — Fear of fever
The Phobia List: R
Radiophobia — Fear of radiation or x-rays
Ranidaphobia — Fear of frogs
Rectophobia — Fear of rectums or rectal diseases
Rhabdophobia — Fear of being severely punished, beaten by a rod, or severely criticized
Rhypophobia — Fear of defecation
Rhytiphobia — Fear of getting wrinkles
Rupophobia — Fear of dirt
Russophobia — Fear of Russians
The Phobia List: S
Samhainophobia — Fear of Halloween
Satanophobia — Fear of Satan or The Devil
Scabiophobia — Fear of scabies
Scelerophibia — Fear of bad men or burglars
Sciaphobia — Fear of shadows
Scoleciphobia — Fear of worms
Scolionophobia — Fear of school
Scopophobia — Fear of being seen or stared at
Scoptophobia — Fear of blindness in visual field
Scriptophobia — Fear of writing in public
Selachophobia — Fear of sharks
Selaphobia — Fear of light flashes
Selenophobia — Fear of the moon
Seplophobia — Fear of decaying matter
Siderodromophobia — Fear of trains, railroads, or train travel
Siderophobia — Fear of stars
Sinistrophobia — Fear of things to the left or left-handed
Sinophobia — Fear of China, Chinese, or Chinese culture
Sitiophobia — Fear of food or eating
Soceraphobia — Fear of parents-in-law
Social Phobia — Fear of social situations
Sociophobia — Fear of society or people in general
Somniphobia — Fear of sleep
Sophophobia — Fear of learning
Soteriophobia — Fear of dependence on others
Spacephobia — Fear of outer space
Spectrophobia — Fear of specters or ghosts
Spheksophobia — Fear of wasps
Stasibasiphobia — Fear of standing or walking
Statue Phobia — Fear of statues or effigies
Staurophobia — Fear of crosses or the crucifix
Stenophobia — Fear of narrow things or places
Symbolophobia — Fear of symbolism
Symmetrophobia — Fear of symmetry
Syngenesophobia — Fear of relatives
The Phobia List: T
Tachophobia — Fear of speed
Taeniophobia — Fear of tapeworms
Taphephobia — Fear of being buried alive or cemeteries
Tapinophobia — Fear of being contagious
Taurophobia — Fear of bulls
Technophobia — Fear of technology or computers
Teleophobia — Fear of definite plans or Religious ceremony
Telephonophobia — Fear of telephones
Teratophobia — Fear of bearing a deformed child, monsters, or deformed people
Testophobia — Fear of taking tests
Tetanophobia — Fear of lockjaw or tetanus
Textophobia — Fear of certain fabrics
Thalassophobia — Fear of the sea or the ocean
Thanatophobia — Fear of death, dying, being buried, cremation, or entombment
Theatrophobia — Fear of theaters
Theologicophobia — Fear of theology
Theophobia — Fear of gods or religion
Thermophobia — Fear of heat
Tocophobia — Fear of pregnancy or childbirth
Tomophobia — Fear of surgery or surgical operations
Topophobia — Fear of fear of certain places or situations
Toxicophobia — Fear of poison or being accidently poisoned
Traumatophobia — Fear of injury or battle
Tremophobia — Fear of trembling
Trichinophobia — Fear of trichinosis
Trichopathophobia — Fear of hair
Triskaidekaphobia — Fear of the number 13
Tropophobia — Fear of moving or making changes
Trypanophobia — Fear of injections
Tyrannophobia — Fear of tyrants
The Phobia List: U
Urophobia — Fear of urine or urinating
The Phobia List: V
Vaccinophobia — Fear of vaccination
Verminophobia — Fear of germs
Vestiphobia — Fear of clothing
Virginitiphobia — Fear of rape
Vitricophobia — Fear of step-father's
The Phobia List: W
Walloonphobia — Fear of the Walloons
Wiccaphobia — Fear of witches and witchcraft
The Phobia List: X
Xanthophobia — Fear of the color yellow or the word yellow
Xenoglossophobia — Fear of foreign languages
Xenophobia — Fear of strangers or foreigners
Xerophobia — Fear of dryness
Xylophobia — Fear of wood, wooden objects, or forests
Xyrophobia — Fear of razors
The Phobia List: Z
Zelophobia — Fear of jealousy
Zemmiphobia — Fear of the great mole rat
Zeusophobia — Fear of God or gods
Zoophobia — Fear of animals
Wednesday, July 30, 2008
Medifast Diet: Complete Review
The Medifast diet plan is popular.
Forbes recently placed the company at number 28 in their 200 best small companies list), and Medifast have even produced a book (What Physicians Have Always Known About Weight Loss).
But what is Medifast all about? One clue is the name - it contains the word fast...
The Basics
The Medifast brand has been around for a number of decades, and at one time was only available via physicians. Nowadays the products can be ordered on-line and through a number of distributors.
Medifast offer a stable of meal replacement products - all generally formulated to be low-calorie and low-fat, and containing the optimum levels of vitamins. The formula will generally take users into a mild state of ketosis.
The most popular plan is called 5 and 1. This plan (800-1000 calories daily) comprises 5 meal replacements and one "real" meal containing a lean protein and vegetables and salad. Medifast claim a weight loss of 2-5 pounds per week on this plan.
Proof?
What many people don't realize is that very few commercial weight loss programs have ever undergone any clinical studies. Medifast heavily promote the fact that a Johns Hopkins university study has shown that Medifast results in significant weight loss (67 pound average loss in males and 57 pound average loss in females). It's worth pointing out that this study looked at patients who attended Medifast clinics.
There is also an additional study that compared the Medifast program with diabetes medication. The study found Medifast more effective at controlling type 2 diabetes than an ADA-recommended program (see PR).
Both studies were led by Associate Professor Lawrence Cheskin of Johns Hopkins Bloomberg School of Public Health and were funded by Medifast.
Successes
Due to the popularity of the program, Medifast have a number of "success stories" - one of which is Nnedi Uzowihe-Igwe of Maryland, USA (currently featured on the Medifast site). She also appeared in People magazine in January 2006 describing a massive transformation that resulted in a 160lb weight loss between June 2004 and April 2005. Nnedi subsequently became pregnant and gave birth to her second daughter)
I was able to find out how Nnedi was going now, and she appears to have maintained her massive initial weight loss (and is aiming to lose the weight she put on with the second baby by the end of this year).
What you can expect
Drastic
Protein fasts and low-calorie meal replacements are a drastic solution, and in my opinion appropriate for drastic situations. Given the choice between gastric bypass surgery or Medifast, then Medifast must surely be a better answer.
The biggest test of a program such as Medifast is the long-term consequences - and in particular weaning off a program based around shakes and soups. The transition phase should be four to six weeks, and often starts off by introducing some oatmeal at breakfast, and some fruit for snacks. Also exercise must become a part of life (5 days a week). Exercise must be fairly low-key during the restrictive part of Medifast - but once transitioning - it becomes increasingly important.
Due to the level of energy intake and exercise levels - it is likely that some muscle loss will occur during the weight loss phase. Once again, the best course of action would be to gradually include strength training during the transition phase - and begin to build up muscle tone.
Costs
The Medifast 5 and 1 plan cost $275 for 4 weeks. However - that's the cost of the "5" - you will still need to buy your daily "lean and green" meal (lean protein plus salad/vegetables).
Men & Women
Different formulations are used for men and women. Some shakes are called Medifast 55 or Medifast 70. The latter has a higher soy protein content and is more suitable for men (or women who prefer higher protein).
Behavior Change Required
Behavioral changes are critical to the long-term success of Medifast. Unless these lifestyle changes are applied, then the weight could easily swing back on like a yo-yo. It's worth taking a look at the post 10 Questions To Ask Before Changing Your Diet.
Conclusion
I don't believe Medifast is for the person who wants to lose 20 pounds. This is a serious program for serious situations, and it may be advisable to follow the program while receiving regular support from a clinic, and even under medical advisement.
However ample proof exists that the program does work and can lead to significant weight loss provided the transition phase is followed correctly.
Forbes recently placed the company at number 28 in their 200 best small companies list), and Medifast have even produced a book (What Physicians Have Always Known About Weight Loss).
But what is Medifast all about? One clue is the name - it contains the word fast...
The Basics
The Medifast brand has been around for a number of decades, and at one time was only available via physicians. Nowadays the products can be ordered on-line and through a number of distributors.
Medifast offer a stable of meal replacement products - all generally formulated to be low-calorie and low-fat, and containing the optimum levels of vitamins. The formula will generally take users into a mild state of ketosis.
The most popular plan is called 5 and 1. This plan (800-1000 calories daily) comprises 5 meal replacements and one "real" meal containing a lean protein and vegetables and salad. Medifast claim a weight loss of 2-5 pounds per week on this plan.
Proof?
What many people don't realize is that very few commercial weight loss programs have ever undergone any clinical studies. Medifast heavily promote the fact that a Johns Hopkins university study has shown that Medifast results in significant weight loss (67 pound average loss in males and 57 pound average loss in females). It's worth pointing out that this study looked at patients who attended Medifast clinics.
There is also an additional study that compared the Medifast program with diabetes medication. The study found Medifast more effective at controlling type 2 diabetes than an ADA-recommended program (see PR).
Both studies were led by Associate Professor Lawrence Cheskin of Johns Hopkins Bloomberg School of Public Health and were funded by Medifast.
Successes
Due to the popularity of the program, Medifast have a number of "success stories" - one of which is Nnedi Uzowihe-Igwe of Maryland, USA (currently featured on the Medifast site). She also appeared in People magazine in January 2006 describing a massive transformation that resulted in a 160lb weight loss between June 2004 and April 2005. Nnedi subsequently became pregnant and gave birth to her second daughter)
I was able to find out how Nnedi was going now, and she appears to have maintained her massive initial weight loss (and is aiming to lose the weight she put on with the second baby by the end of this year).
What you can expect
Drastic
Protein fasts and low-calorie meal replacements are a drastic solution, and in my opinion appropriate for drastic situations. Given the choice between gastric bypass surgery or Medifast, then Medifast must surely be a better answer.
The biggest test of a program such as Medifast is the long-term consequences - and in particular weaning off a program based around shakes and soups. The transition phase should be four to six weeks, and often starts off by introducing some oatmeal at breakfast, and some fruit for snacks. Also exercise must become a part of life (5 days a week). Exercise must be fairly low-key during the restrictive part of Medifast - but once transitioning - it becomes increasingly important.
Due to the level of energy intake and exercise levels - it is likely that some muscle loss will occur during the weight loss phase. Once again, the best course of action would be to gradually include strength training during the transition phase - and begin to build up muscle tone.
Costs
The Medifast 5 and 1 plan cost $275 for 4 weeks. However - that's the cost of the "5" - you will still need to buy your daily "lean and green" meal (lean protein plus salad/vegetables).
Men & Women
Different formulations are used for men and women. Some shakes are called Medifast 55 or Medifast 70. The latter has a higher soy protein content and is more suitable for men (or women who prefer higher protein).
Behavior Change Required
Behavioral changes are critical to the long-term success of Medifast. Unless these lifestyle changes are applied, then the weight could easily swing back on like a yo-yo. It's worth taking a look at the post 10 Questions To Ask Before Changing Your Diet.
Conclusion
I don't believe Medifast is for the person who wants to lose 20 pounds. This is a serious program for serious situations, and it may be advisable to follow the program while receiving regular support from a clinic, and even under medical advisement.
However ample proof exists that the program does work and can lead to significant weight loss provided the transition phase is followed correctly.
The Best Acne Treatments
There are too many acne fighting products on the market to count, and the majority of them simply do not work. However, there are some that do work quite well. The problem is that many people who suffer from acne will spend quite a bit of time and money trying to find the best acne treatments. Teenagers often outgrow acne before they find a treatment that works.
One of the better acne treatments on the market today is ProActiv. ProActiv seems to be helping many people who could not find other solutions that worked. It has been featured on infomercials, news stories, magazine articles, and newspaper articles. Proactiv is a system that includes a renewing cleanser, revitalizing toner, and repairing lotion. Prescription grade benzoyl peroxide is the active ingredient in ProActiv. ProActiv does not require a prescription.
A treatment that is available by prescription is Accutane. Accutane is a very strong medication, that is only suitable for those who suffer from severe and persistent acne. The medication is taken internally, and there are possible side effects, including birth defects, dry and cracked lips, and liver dysfunction.
Another one of that is used topically is retin-a. Many people have had great success with retin-a, which is used to treat acne, acne scars, wrinkles, stretch marks, skin discoloration, and a variety of other skin afflictions. Retin-a is available by prescription, but some over the counter medications contain retin-a.
Not all treatments come in the form of chemicals. Certain essential oils are also beneficial in the treatment of acne. These essential oils can be applied topically for the treatment of mild to moderate acne. The best essential oils for acne treatment are: Tea Tree Oil, Bergamot Oil, Clove Oil, Lavender Oil, and Rosewood Oil. If the essential oil needs to be diluted, mix it with Grapeseed Oil for best results.
In order to find the best acne treatment for you, start with essential oils. If that doesn't work, go to the next step by trying ProActive. If ProActive doesn't work, then try a prescription alternative. You may also consider being tested for food allergies, as certain allergies can cause acne. In this case, the only treatment you need is to eliminate those certain foods from your diet.
One of the better acne treatments on the market today is ProActiv. ProActiv seems to be helping many people who could not find other solutions that worked. It has been featured on infomercials, news stories, magazine articles, and newspaper articles. Proactiv is a system that includes a renewing cleanser, revitalizing toner, and repairing lotion. Prescription grade benzoyl peroxide is the active ingredient in ProActiv. ProActiv does not require a prescription.
A treatment that is available by prescription is Accutane. Accutane is a very strong medication, that is only suitable for those who suffer from severe and persistent acne. The medication is taken internally, and there are possible side effects, including birth defects, dry and cracked lips, and liver dysfunction.
Another one of that is used topically is retin-a. Many people have had great success with retin-a, which is used to treat acne, acne scars, wrinkles, stretch marks, skin discoloration, and a variety of other skin afflictions. Retin-a is available by prescription, but some over the counter medications contain retin-a.
Not all treatments come in the form of chemicals. Certain essential oils are also beneficial in the treatment of acne. These essential oils can be applied topically for the treatment of mild to moderate acne. The best essential oils for acne treatment are: Tea Tree Oil, Bergamot Oil, Clove Oil, Lavender Oil, and Rosewood Oil. If the essential oil needs to be diluted, mix it with Grapeseed Oil for best results.
In order to find the best acne treatment for you, start with essential oils. If that doesn't work, go to the next step by trying ProActive. If ProActive doesn't work, then try a prescription alternative. You may also consider being tested for food allergies, as certain allergies can cause acne. In this case, the only treatment you need is to eliminate those certain foods from your diet.
Pick disease
form of premature dementia caused by atrophy of the frontal and temporal lobes of the brain. It resembles Alzheimer disease but is much less common. Pick disease is characterized by a progressive deterioration of intellect, judgment, and memory, resulting in increased irritability, inappropriate behaviour, depression, and paranoia. Histologically some cerebral nerve cells are swollen and contain abnormal inclusions called Pick bodies. The cause of Pick disease is unknown, but in some cases the disease appears to be inherited. Average survival from onset (generally between the ages of 40 and 60) to death is about 10 years; there is no specific treatment. The disease was first described by the German neurologist Arnold Pick.
Asthma
Asthma is a chronic condition involving the respiratory system in which the airways occasionally constrict, become inflamed, and are lined with excessive amounts of mucus, often in response to one or more triggers.[1] These episodes may be triggered by such things as exposure to an environmental stimulant such as an allergen, environmental tobacco smoke, cold or warm air, perfume, pet dander, moist air, exercise or exertion, or emotional stress. In children, the most common triggers are viral illnesses such as those that cause the common cold.[2] This airway narrowing causes symptoms such as wheezing, shortness of breath, chest tightness, and coughing. The airway constriction responds to bronchodilators. Between episodes, most patients feel well but can have mild symptoms and they may remain short of breath after exercise for longer periods of time than the unaffected individual. The symptoms of asthma, which can range from mild to life threatening, can usually be controlled with a combination of drugs and environmental changes.
Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.
Signs and symptoms
In some individuals asthma is characterized by chronic respiratory impairment. In others it is an intermittent illness marked by episodic symptoms that may result from a number of triggering events, including upper respiratory infection, stress, airborne allergens, air pollutants (such as smoke or traffic fumes), or exercise. Some or all of the following symptoms may be present in those with asthma: dyspnea, wheezing, stridor, coughing, an inability for physical exertion. Some asthmatics who have severe shortness of breath and tightening of the lungs never wheeze or have stridor and their symptoms may be confused with a COPD-type disease.
An acute exacerbation of asthma is commonly referred to as an asthma attack. The clinical hallmarks of an attack are shortness of breath (dyspnea) and either wheezing or stridor.[4] Although the former is "often regarded as the sine qua non of asthma",[4] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard. When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in both respiratory phases).
Signs of an asthmatic episode include wheezing, prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. During a serious asthma attack, the accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used, shown as in-drawing of tissues between the ribs and above the sternum and clavicles.
During very severe attacks, an asthma sufferer can turn blue from lack of oxygen, and can experience chest pain or even loss of consciousness. Just before loss of consciousness, there is a chance that the patient will feel numbness in the limbs and palms may start to sweat. The person's feet may become icy cold. Severe asthma attacks, which may not be responsive to standard treatments (status asthmaticus), are life-threatening and may lead to respiratory arrest and death. Despite the severity of symptoms during an asthmatic episode, between attacks an asthmatic may show few or even no signs of the disease.[5]
Cause
Asthma is caused by a complex interaction of environmental and genetic factors that researchers do not fully understand yet.[6] These factors can also influence how severe a person’s asthma is and how well they respond to medication.[7] As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all of them have been replicated. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may only affect asthma when combined.
Environmental
Many environmental risk factors have been associated with asthma, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association:
* Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[8][9]
* Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[8]
* Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.[8][10][11]
* Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[12]
* Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).[13]
* Psychological stress on the part of a child's caregiver has been associated with asthma, and is an area of active research. Stress can modify behaviors that affect asthma, like smoking, but research suggests that stress has other effects as well. There is growing evidence that stress may influence asthma and other diseases by influencing the immune system.[8]
The hygiene hypothesis is a theory about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, c-sections, and cleaning products.[12][13][14] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.
Genetic
Over 100 genes have been associated with asthma in at least one genetic association study.[15] However, as with all association studies, replication is important before genetic variation (such as a single nucleotide polymorphism, or SNP) in a certain gene is thought to influence asthma. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[15]
* GSTM1
* IL10
* CTLA4
* SPINK5
* LTC4S
* LTA
* GRPA
* NOD1
* CC16
* GSTP1
* STAT6
* NOS1
* CCL5
* TBXA2R
* TGFB1
* IL4
* IL13
* CD14
* ADRB2 (β-2 adrenergic receptor)
* HLA-DRB1
* HLA-DQB1
* TNF
* FCER1B
* IL4R
* ADAM33
Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[15] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma.
Stimuli
# Allergens from nature, typically inhaled, which include waste from common household pests, such as the house dust mite and cockroach, grass pollen, mould spores, and pet epithelial cells;[citation needed]
# Indoor air pollution from volatile organic compounds, including perfumes and perfumed products. Examples include soap, dishwashing liquid, laundry detergent, fabric softener, paper tissues, paper towels, toilet paper, shampoo, hairspray, hair gel, cosmetics, facial cream, sun cream, deodorant, cologne, shaving cream, aftershave lotion, air freshener and candles, and products such as oil-based paint.[citation needed]
# Medications, including aspirin,[18] β-adrenergic antagonists (beta blockers), and penicillin.[citation needed]
# Food allergies such as milk, peanuts, and eggs. However, asthma is rarely the only symptom, and not all people with food or other allergies have asthma.[citation needed]
# Use of fossil fuel related allergenic air pollution, such as ozone, smog, summer smog, nitrogen dioxide, and sulfur dioxide, which is thought to be one of the major reasons for the high prevalence of asthma in urban areas.[citation needed]
# Various industrial compounds and other chemicals, notably sulfites; chlorinated swimming pools generate chloramines—monochloramine (NH2Cl), dichloramine (NHCl2) and trichloramine (NCl3)—in the air around them, which are known to induce asthma.[19]
# Early childhood infections, especially viral respiratory infections. However, persons of any age can have asthma triggered by colds and other respiratory infections even though their normal stimuli might be from another category (e.g. pollen) and absent at the time of infection. In many cases, significant asthma may not even occur until the respiratory infection is in its waning stage, and the person is seemingly improving. Eighty percent of asthma attacks in adults and 60% in children are caused by respiratory viruses.[citation needed]
# Exercise or intense use of respiratory system. The effects of which differ somewhat from those of the other triggers, since they are brief. It is known that exercising regularly actually helps to cure asthma.[citation needed]
# Hormonal changes in adolescent girls and adult women associated with their menstrual cycle can lead to a worsening of asthma. Some women also experience a worsening of their asthma during pregnancy whereas others find no significant changes, and in other women their asthma improves during their pregnancy.[citation needed]
# Emotional stress which is poorly understood as a trigger.[citation needed] Emotional stress can affect breathing temporarily, however unlike something such as heart problems, it is unclear if it has any long-term effect.
# Cold weather can make it harder for asthmatics to breathe.[20] Whether high altitude helps or worsens asthma is debatable and may vary from person to person.
Pathogenesis
The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis: the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.
In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma.[22] Szentivanyi's Beta Adrenergic Theory is a citation classic[23] and has been cited more times than any other article in the history of the Journal of Allergy.
In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors.[24] Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergy.[25]
The Beta-Adrenergic Theory has been cited in the scholarship of such noted investigators as Richard F. Lockey (former President of the American Academy of Allergy, Asthma, and Immunology),[26] Charles Reed (Chief of Allergy at Mayo Medical School),[27] and Craig Venter (Human Genome Project).[28]
John P. McGovern, President of the American Association of Allergy nominated Szentivanyi for The 1968 Nobel Prize in Medicine in recognition of The Beta Adrenergic Theory.
In 2006, Researchers at Harvard Medical School found evidence that asthma is caused by over-proliferation of a special type of natural "killer" cell.
Diagnosis
Asthma is defined simply as reversible airway obstruction. Reversibility occurs either spontaneously or with treatment. The basic measurement is peak flow rates and the following diagnostic criteria are used by the British Thoracic Society:[33]
* ≥20% difference on at least three days in a week for at least two weeks;
* ≥20% improvement of peak flow following treatment, for example:
o 10 minutes of inhaled β-agonist (e.g., salbutamol);
o six week of inhaled corticosteroid (e.g., beclometasone);
o 14 days of 30mg prednisolone.
* ≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).
In many cases, a physician can diagnose asthma on the basis of typical findings in a patient's clinical history and examination. Asthma is strongly suspected if a patient suffers from eczema or other allergic conditions—suggesting a general atopic constitution—or has a family history of asthma. While measurement of airway function is possible for adults, most new cases are diagnosed in children who are unable to perform such tests. Diagnosis in children is based on a careful compilation and analysis of the patient's medical history and subsequent improvement with an inhaled bronchodilator medication. In adults, diagnosis can be made with a peak flow meter (which tests airway restriction), looking at both the diurnal variation and any reversibility following inhaled bronchodilator medication.
Testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young asthmatics who may experience only exercise-induced asthma. If the diagnosis is in doubt, a more formal lung function test may be conducted. Once a diagnosis of asthma is made, a patient can use peak flow meter testing to monitor the severity of the disease.
Monitoring asthma with a peak flow meter on an ongoing basis assists with self monitoring of asthma. Peak flow readings can be charted on graph paper charts together with a record of symptoms or use peak flow charting software.[34] This allows patients to track their peak flow readings and pass information back to their doctor or nurse.[35]
In the Emergency Department doctors may use a capnography which measures the amount of exhaled carbon dioxide,[36] along with pulse oximetry which shows the amount of oxygen dissolved in the blood, to determine the severity of an asthma attack as well as the response to treatment.
More recently, exhaled nitric oxide has been studied as a breath test indicative of airway inflammation in asthma.
Prevention
Current treatment protocols recommend prevention medications such as an inhaled corticosteroid, which helps to suppress inflammation and reduces the swelling of the lining of the airways, in anyone who has frequent (greater than twice a week) need of relievers or who has severe symptoms. If symptoms persist, additional preventive drugs are added until the asthma is controlled. With the proper use of prevention drugs, asthmatics can avoid the complications that result from overuse of relief medications.
Asthmatics sometimes stop taking their preventive medication when they feel fine and have no problems breathing. This often results in further attacks, and no long-term improvement.
Preventive agents include the following.
* Inhaled glucocorticoids are the most widely used of the prevention medications and normally come as inhaler devices (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone).
Long-term use of corticosteroids can have many side effects including a redistribution of fat, increased appetite, blood glucose problems and weight gain. In particular high doses of steroids may cause osteoporosis. For this reasons inhaled steroids are generally used for prevention, as their smaller doses are targeted to the lungs unlike the higher doses of oral preparations. Nevertheless, patients on high doses of inhaled steroids may still require prophylactic treatment to prevent osteoporosis.
Deposition of steroids in the mouth may cause a hoarse voice or oral thrush (due to decreased immunity). This may be minimised by rinsing the mouth with water after inhaler use, as well as by using a spacer which increases the amount of drug that reaches the lungs.
* Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton).
* Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil).
* Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium), which have a mixed reliever and preventer effect. (These are rarely used in preventive treatment of asthma, except in patients who do not tolerate beta-2-agonists.)
* Methylxanthines (theophylline and aminophylline), which are sometimes considered if sufficient control cannot be achieved with inhaled glucocorticoids and long-acting β-agonists alone.
* Antihistamines, often used to treat allergic symptoms that may underlie the chronic inflammation.
* Hyposensitization, (also known as immunodesensitisation therapy) may be recommended in some cases where allergy is the suspected cause or trigger of asthma. Depending on the allergen, it can be given orally or by injection.
* Omalizumab, an IgE blocker; this can help patients with severe allergic asthma that does not respond to other drugs. However, it is expensive and must be injected.
* Methotrexate is occasionally used in some difficult-to-treat patients.
* If chronic acid indigestion (GERD) contributes to a patient's asthma, it should also be treated, because it may prolong the respiratory problem.
Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.
Signs and symptoms
In some individuals asthma is characterized by chronic respiratory impairment. In others it is an intermittent illness marked by episodic symptoms that may result from a number of triggering events, including upper respiratory infection, stress, airborne allergens, air pollutants (such as smoke or traffic fumes), or exercise. Some or all of the following symptoms may be present in those with asthma: dyspnea, wheezing, stridor, coughing, an inability for physical exertion. Some asthmatics who have severe shortness of breath and tightening of the lungs never wheeze or have stridor and their symptoms may be confused with a COPD-type disease.
An acute exacerbation of asthma is commonly referred to as an asthma attack. The clinical hallmarks of an attack are shortness of breath (dyspnea) and either wheezing or stridor.[4] Although the former is "often regarded as the sine qua non of asthma",[4] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard. When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in both respiratory phases).
Signs of an asthmatic episode include wheezing, prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. During a serious asthma attack, the accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used, shown as in-drawing of tissues between the ribs and above the sternum and clavicles.
During very severe attacks, an asthma sufferer can turn blue from lack of oxygen, and can experience chest pain or even loss of consciousness. Just before loss of consciousness, there is a chance that the patient will feel numbness in the limbs and palms may start to sweat. The person's feet may become icy cold. Severe asthma attacks, which may not be responsive to standard treatments (status asthmaticus), are life-threatening and may lead to respiratory arrest and death. Despite the severity of symptoms during an asthmatic episode, between attacks an asthmatic may show few or even no signs of the disease.[5]
Cause
Asthma is caused by a complex interaction of environmental and genetic factors that researchers do not fully understand yet.[6] These factors can also influence how severe a person’s asthma is and how well they respond to medication.[7] As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all of them have been replicated. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may only affect asthma when combined.
Environmental
Many environmental risk factors have been associated with asthma, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association:
* Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[8][9]
* Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[8]
* Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.[8][10][11]
* Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[12]
* Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).[13]
* Psychological stress on the part of a child's caregiver has been associated with asthma, and is an area of active research. Stress can modify behaviors that affect asthma, like smoking, but research suggests that stress has other effects as well. There is growing evidence that stress may influence asthma and other diseases by influencing the immune system.[8]
The hygiene hypothesis is a theory about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, c-sections, and cleaning products.[12][13][14] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.
Genetic
Over 100 genes have been associated with asthma in at least one genetic association study.[15] However, as with all association studies, replication is important before genetic variation (such as a single nucleotide polymorphism, or SNP) in a certain gene is thought to influence asthma. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[15]
* GSTM1
* IL10
* CTLA4
* SPINK5
* LTC4S
* LTA
* GRPA
* NOD1
* CC16
* GSTP1
* STAT6
* NOS1
* CCL5
* TBXA2R
* TGFB1
* IL4
* IL13
* CD14
* ADRB2 (β-2 adrenergic receptor)
* HLA-DRB1
* HLA-DQB1
* TNF
* FCER1B
* IL4R
* ADAM33
Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[15] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma.
Stimuli
# Allergens from nature, typically inhaled, which include waste from common household pests, such as the house dust mite and cockroach, grass pollen, mould spores, and pet epithelial cells;[citation needed]
# Indoor air pollution from volatile organic compounds, including perfumes and perfumed products. Examples include soap, dishwashing liquid, laundry detergent, fabric softener, paper tissues, paper towels, toilet paper, shampoo, hairspray, hair gel, cosmetics, facial cream, sun cream, deodorant, cologne, shaving cream, aftershave lotion, air freshener and candles, and products such as oil-based paint.[citation needed]
# Medications, including aspirin,[18] β-adrenergic antagonists (beta blockers), and penicillin.[citation needed]
# Food allergies such as milk, peanuts, and eggs. However, asthma is rarely the only symptom, and not all people with food or other allergies have asthma.[citation needed]
# Use of fossil fuel related allergenic air pollution, such as ozone, smog, summer smog, nitrogen dioxide, and sulfur dioxide, which is thought to be one of the major reasons for the high prevalence of asthma in urban areas.[citation needed]
# Various industrial compounds and other chemicals, notably sulfites; chlorinated swimming pools generate chloramines—monochloramine (NH2Cl), dichloramine (NHCl2) and trichloramine (NCl3)—in the air around them, which are known to induce asthma.[19]
# Early childhood infections, especially viral respiratory infections. However, persons of any age can have asthma triggered by colds and other respiratory infections even though their normal stimuli might be from another category (e.g. pollen) and absent at the time of infection. In many cases, significant asthma may not even occur until the respiratory infection is in its waning stage, and the person is seemingly improving. Eighty percent of asthma attacks in adults and 60% in children are caused by respiratory viruses.[citation needed]
# Exercise or intense use of respiratory system. The effects of which differ somewhat from those of the other triggers, since they are brief. It is known that exercising regularly actually helps to cure asthma.[citation needed]
# Hormonal changes in adolescent girls and adult women associated with their menstrual cycle can lead to a worsening of asthma. Some women also experience a worsening of their asthma during pregnancy whereas others find no significant changes, and in other women their asthma improves during their pregnancy.[citation needed]
# Emotional stress which is poorly understood as a trigger.[citation needed] Emotional stress can affect breathing temporarily, however unlike something such as heart problems, it is unclear if it has any long-term effect.
# Cold weather can make it harder for asthmatics to breathe.[20] Whether high altitude helps or worsens asthma is debatable and may vary from person to person.
Pathogenesis
The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis: the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.
In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma.[22] Szentivanyi's Beta Adrenergic Theory is a citation classic[23] and has been cited more times than any other article in the history of the Journal of Allergy.
In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors.[24] Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergy.[25]
The Beta-Adrenergic Theory has been cited in the scholarship of such noted investigators as Richard F. Lockey (former President of the American Academy of Allergy, Asthma, and Immunology),[26] Charles Reed (Chief of Allergy at Mayo Medical School),[27] and Craig Venter (Human Genome Project).[28]
John P. McGovern, President of the American Association of Allergy nominated Szentivanyi for The 1968 Nobel Prize in Medicine in recognition of The Beta Adrenergic Theory.
In 2006, Researchers at Harvard Medical School found evidence that asthma is caused by over-proliferation of a special type of natural "killer" cell.
Diagnosis
Asthma is defined simply as reversible airway obstruction. Reversibility occurs either spontaneously or with treatment. The basic measurement is peak flow rates and the following diagnostic criteria are used by the British Thoracic Society:[33]
* ≥20% difference on at least three days in a week for at least two weeks;
* ≥20% improvement of peak flow following treatment, for example:
o 10 minutes of inhaled β-agonist (e.g., salbutamol);
o six week of inhaled corticosteroid (e.g., beclometasone);
o 14 days of 30mg prednisolone.
* ≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).
In many cases, a physician can diagnose asthma on the basis of typical findings in a patient's clinical history and examination. Asthma is strongly suspected if a patient suffers from eczema or other allergic conditions—suggesting a general atopic constitution—or has a family history of asthma. While measurement of airway function is possible for adults, most new cases are diagnosed in children who are unable to perform such tests. Diagnosis in children is based on a careful compilation and analysis of the patient's medical history and subsequent improvement with an inhaled bronchodilator medication. In adults, diagnosis can be made with a peak flow meter (which tests airway restriction), looking at both the diurnal variation and any reversibility following inhaled bronchodilator medication.
Testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young asthmatics who may experience only exercise-induced asthma. If the diagnosis is in doubt, a more formal lung function test may be conducted. Once a diagnosis of asthma is made, a patient can use peak flow meter testing to monitor the severity of the disease.
Monitoring asthma with a peak flow meter on an ongoing basis assists with self monitoring of asthma. Peak flow readings can be charted on graph paper charts together with a record of symptoms or use peak flow charting software.[34] This allows patients to track their peak flow readings and pass information back to their doctor or nurse.[35]
In the Emergency Department doctors may use a capnography which measures the amount of exhaled carbon dioxide,[36] along with pulse oximetry which shows the amount of oxygen dissolved in the blood, to determine the severity of an asthma attack as well as the response to treatment.
More recently, exhaled nitric oxide has been studied as a breath test indicative of airway inflammation in asthma.
Prevention
Current treatment protocols recommend prevention medications such as an inhaled corticosteroid, which helps to suppress inflammation and reduces the swelling of the lining of the airways, in anyone who has frequent (greater than twice a week) need of relievers or who has severe symptoms. If symptoms persist, additional preventive drugs are added until the asthma is controlled. With the proper use of prevention drugs, asthmatics can avoid the complications that result from overuse of relief medications.
Asthmatics sometimes stop taking their preventive medication when they feel fine and have no problems breathing. This often results in further attacks, and no long-term improvement.
Preventive agents include the following.
* Inhaled glucocorticoids are the most widely used of the prevention medications and normally come as inhaler devices (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone).
Long-term use of corticosteroids can have many side effects including a redistribution of fat, increased appetite, blood glucose problems and weight gain. In particular high doses of steroids may cause osteoporosis. For this reasons inhaled steroids are generally used for prevention, as their smaller doses are targeted to the lungs unlike the higher doses of oral preparations. Nevertheless, patients on high doses of inhaled steroids may still require prophylactic treatment to prevent osteoporosis.
Deposition of steroids in the mouth may cause a hoarse voice or oral thrush (due to decreased immunity). This may be minimised by rinsing the mouth with water after inhaler use, as well as by using a spacer which increases the amount of drug that reaches the lungs.
* Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton).
* Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil).
* Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium), which have a mixed reliever and preventer effect. (These are rarely used in preventive treatment of asthma, except in patients who do not tolerate beta-2-agonists.)
* Methylxanthines (theophylline and aminophylline), which are sometimes considered if sufficient control cannot be achieved with inhaled glucocorticoids and long-acting β-agonists alone.
* Antihistamines, often used to treat allergic symptoms that may underlie the chronic inflammation.
* Hyposensitization, (also known as immunodesensitisation therapy) may be recommended in some cases where allergy is the suspected cause or trigger of asthma. Depending on the allergen, it can be given orally or by injection.
* Omalizumab, an IgE blocker; this can help patients with severe allergic asthma that does not respond to other drugs. However, it is expensive and must be injected.
* Methotrexate is occasionally used in some difficult-to-treat patients.
* If chronic acid indigestion (GERD) contributes to a patient's asthma, it should also be treated, because it may prolong the respiratory problem.
Sunday, June 15, 2008
Disease from tsetse fly
In the tropical regions of Africa, the bloodsucking tsetse fly carries deadly diseases to humans and other animals. It is a brownish-colored insect, only a little larger than the common housefly. When it is at rest its wings close flat on the back and are completely overlapping, whereas those of the housefly are held somewhat erect and spread. There are 21 known species of the tsetse fly. Some carry the disease trypanosomiasis (African sleeping sickness) from one human victim to another. Others carry the disease nagana to cattle and other animals.
When the fly bites an infected victim, the insect draws into its own bloodstream a parasite called a trypanosome. After going through a stage of development in the fly, the parasite is transferred to the next victim. Thus the disease, caused by the parasite, is passed from person to person, from animal to animal, through the bite of the fly. The disease is so called because in the last stages of the illness the victim falls into a sleep, which often ends in death.
The tsetse fly breeds in brushy places in tropical forests and on the edges of rivers and lakes. The female, unlike most insects, does not lay eggs. Instead, she deposits on the ground a single full-grown larva at intervals of about two weeks. The larva hides in brush and immediately goes into the pupal stage, from which it emerges as a mature fly.
Tsetse flies belong to the genus Glossina of the family Glossinidae, which is related to the Muscidae. The scientific name of the commonest carrier of African sleeping sickness is G. palpalis. The principal carrier of nagana is G. morsitans.
When the fly bites an infected victim, the insect draws into its own bloodstream a parasite called a trypanosome. After going through a stage of development in the fly, the parasite is transferred to the next victim. Thus the disease, caused by the parasite, is passed from person to person, from animal to animal, through the bite of the fly. The disease is so called because in the last stages of the illness the victim falls into a sleep, which often ends in death.
The tsetse fly breeds in brushy places in tropical forests and on the edges of rivers and lakes. The female, unlike most insects, does not lay eggs. Instead, she deposits on the ground a single full-grown larva at intervals of about two weeks. The larva hides in brush and immediately goes into the pupal stage, from which it emerges as a mature fly.
Tsetse flies belong to the genus Glossina of the family Glossinidae, which is related to the Muscidae. The scientific name of the commonest carrier of African sleeping sickness is G. palpalis. The principal carrier of nagana is G. morsitans.
Kawasaki disease
rare disease of lymph nodes that causes acquired heart disease in children usually under age 5; characterized by prolonged fever, changes in lips and mouth, swelling of cervical lymph nodes, skin rash, reddening and swelling of hands and feet, and coronary artery damage; may be caused by virus; usually treated with high doses of aspirin; most children conquer fever and rash, but about 20 percent have weakened hearts after the disease.
Newcastle disease
(ND), an influenza-like viral infection of birds that causes epidemics in domestic poultry, and which can spread to humans. The disease was first seen in the English city of Newcastle. It is caused by a single-stranded RNA virus belonging to the viral family Paramyxoviridae. The ND virus is quite stable and can remain infectious for long periods even at low temperature. Newcastle disease is sometimes called avian influenza, but should not be confused with the true influenza strains that infect poultry.
Both wild and pet birds may contract the ND virus. Chickens are among the most susceptible birds; their eggs may also be infected, but can be made safe by heating. The most dangerous strains of the virus, which are rare in the United States, may cause severe illness in birds, including pneumonia, gastrointestinal disease, or encephalitis (inflammation of the brain) leading to paralysis. In chickens and turkeys the disease may be so severe that nearly all those in an infected flock die within three days before any signs of illness have developed. In pet birds the disease ranges from very mild to severe.
Newcastle disease is transmitted by contact with infected birds themselves, which emit the virus when breathing, or with infected products, clothing, feed, and even farm equipment. Once ND is established it is essential to thoroughly disinfect all contaminated objects using strong chemicals.
Newcastle disease is a zoonosis, a disease normally occurring in animals that is communicable to humans. Illness in humans can result from close contact with infectious birds, but is most frequent in persons who work in laboratories where samples from infected birds are analyzed. Generally, headaches and flulike symptoms develop and last four to seven days. A mild, superficial inflammation of the eyes with reddening (conjunctivitis) is common. In humans infected by the virus serious illness or permanent vision impairment is rare. When a pet bird develops ND, the owner should be aware that it may continue to shed the virus, or be contagious, for several months.
Both wild and pet birds may contract the ND virus. Chickens are among the most susceptible birds; their eggs may also be infected, but can be made safe by heating. The most dangerous strains of the virus, which are rare in the United States, may cause severe illness in birds, including pneumonia, gastrointestinal disease, or encephalitis (inflammation of the brain) leading to paralysis. In chickens and turkeys the disease may be so severe that nearly all those in an infected flock die within three days before any signs of illness have developed. In pet birds the disease ranges from very mild to severe.
Newcastle disease is transmitted by contact with infected birds themselves, which emit the virus when breathing, or with infected products, clothing, feed, and even farm equipment. Once ND is established it is essential to thoroughly disinfect all contaminated objects using strong chemicals.
Newcastle disease is a zoonosis, a disease normally occurring in animals that is communicable to humans. Illness in humans can result from close contact with infectious birds, but is most frequent in persons who work in laboratories where samples from infected birds are analyzed. Generally, headaches and flulike symptoms develop and last four to seven days. A mild, superficial inflammation of the eyes with reddening (conjunctivitis) is common. In humans infected by the virus serious illness or permanent vision impairment is rare. When a pet bird develops ND, the owner should be aware that it may continue to shed the virus, or be contagious, for several months.
Tay-Sachs disease
a recessive disorder most common among persons of Middle and Eastern European Jewish origin, and detectable by prenatal tests. Infants appear normal at birth but become listless and inattentive during the first few months of life. An early sign is an exaggerated startle response to sound. Rapidly progressive symptoms include retardation, paralysis, blindness, seizures, and cherry-red retinal spots; death by age 3 is common. Tay-Sachs disease is caused by abnormally low activity of the enzyme hexosaminidase A, resulting in the formation of sphingolipids in the brain
Some diseases of Cats
A good veterinarian is of primary importance to any pet owner. Cat owners should choose a veterinarian who is interested in cats and has treated them successfully. Call a veterinarian at once for advice if a cat seems ill; never try to diagnose a disease or treat the animal yourself.
The most widespread and serious infectious disease of cats is panleucopenia—often called cat distemper, viral enteritis, or cat typhoid. Its onset is sudden and severe, with reduced activity, fever, loss of appetite, and vomiting of yellow fluid. Every cat should be immunized to protect against this disease. The first vaccination is usually given when the animal is about ten weeks old, and boosters should be given annually.
Upper respiratory infections are exceedingly common, and the best-known are pneumonitis and rhinotracheitis. Symptoms resemble those of the common cold in humans and distemper in dogs. The cat's “colds,” however, cannot be passed on to humans or dogs although they are highly infectious for other cats.
Rabies is an invariably fatal viral disease. It is transmitted by the bite of a rabid animal. Rabies has become established among the wild animals in many parts of the world. A cat that roams outdoors in an area where rabies occurs may be bitten by a rabid animal. It is therefore advisable that all cats in such areas be given preventive vaccinations.
A cat that swallows large amounts of fur while grooming may develop fur balls or hair balls. Occasionally these may cause ulcers or completely obstruct the digestive tract. Prevention, in the form of frequent combing and brushing, is best. If fur balls occur in spite of grooming, the animal may be given a teaspoonful of mineral oil in its food or a dab of petroleum jelly on its paws twice a week.
Bite wounds may become infected and cause serious problems. Contrary to popular belief, the cat cannot heal the wound by licking it. It is better to seek veterinary attention as soon as possible.
Many apparently normal cats have tiny mineral crystals in their urine. For reasons not yet fully understood, these crystals often clump together to form sandlike particles or small stones which may cause irritation or obstruction of the urinary passages. A urinary obstruction is a grave emergency and must be treated immediately by a veterinarian.
Ear irritations are most often caused by mites, which are tiny parasites about as large as the point of a pin. The insides of the ears look as though they are filled with a dry brown dirt. The cat shakes its head often and may scratch the outside of the ears and neck persistently. A few drops of any mild oil massaged into the ear canal suffocates the mites and loosens the dirt, which may then be removed with cotton-tipped sticks.
Any cat may get fleas. These small jumping insects live in the cat's fur and suck blood through the animal's skin. Products for treatment are readily available, but use only a preparation labeled safe for cats, and use it strictly as directed.
Worms are a common intestinal parasite of cats. An owner should never try to worm a cat without the advice of a veterinarian. There are several different types of worms, each requiring a different kind of drug for control.
Ringworm, a fungal skin disease, is probably the only infection that is clearly and commonly passed from cat to man. Simple sanitary measures such as keeping pets off the table and washing the hands after handling a cat eliminate most possible risks.
Cats may be poisoned by a variety of substances. They may eat poisonous plants—which include rhododendron, hyacinth, poinsettia, and ivy. Waxes, cleaning fluids, disinfectants, detergents, and mothballs may be toxic or irritating. Antifreeze, weed killers, insecticides, and rodent poisons are outdoor hazards. Cats react adversely to many chemicals and drugs, such as aspirin or iodine, that are safe for humans or other animals. They should never be given medicines not labeled safe for cats or prescribed by a veterinarian.
The most widespread and serious infectious disease of cats is panleucopenia—often called cat distemper, viral enteritis, or cat typhoid. Its onset is sudden and severe, with reduced activity, fever, loss of appetite, and vomiting of yellow fluid. Every cat should be immunized to protect against this disease. The first vaccination is usually given when the animal is about ten weeks old, and boosters should be given annually.
Upper respiratory infections are exceedingly common, and the best-known are pneumonitis and rhinotracheitis. Symptoms resemble those of the common cold in humans and distemper in dogs. The cat's “colds,” however, cannot be passed on to humans or dogs although they are highly infectious for other cats.
Rabies is an invariably fatal viral disease. It is transmitted by the bite of a rabid animal. Rabies has become established among the wild animals in many parts of the world. A cat that roams outdoors in an area where rabies occurs may be bitten by a rabid animal. It is therefore advisable that all cats in such areas be given preventive vaccinations.
A cat that swallows large amounts of fur while grooming may develop fur balls or hair balls. Occasionally these may cause ulcers or completely obstruct the digestive tract. Prevention, in the form of frequent combing and brushing, is best. If fur balls occur in spite of grooming, the animal may be given a teaspoonful of mineral oil in its food or a dab of petroleum jelly on its paws twice a week.
Bite wounds may become infected and cause serious problems. Contrary to popular belief, the cat cannot heal the wound by licking it. It is better to seek veterinary attention as soon as possible.
Many apparently normal cats have tiny mineral crystals in their urine. For reasons not yet fully understood, these crystals often clump together to form sandlike particles or small stones which may cause irritation or obstruction of the urinary passages. A urinary obstruction is a grave emergency and must be treated immediately by a veterinarian.
Ear irritations are most often caused by mites, which are tiny parasites about as large as the point of a pin. The insides of the ears look as though they are filled with a dry brown dirt. The cat shakes its head often and may scratch the outside of the ears and neck persistently. A few drops of any mild oil massaged into the ear canal suffocates the mites and loosens the dirt, which may then be removed with cotton-tipped sticks.
Any cat may get fleas. These small jumping insects live in the cat's fur and suck blood through the animal's skin. Products for treatment are readily available, but use only a preparation labeled safe for cats, and use it strictly as directed.
Worms are a common intestinal parasite of cats. An owner should never try to worm a cat without the advice of a veterinarian. There are several different types of worms, each requiring a different kind of drug for control.
Ringworm, a fungal skin disease, is probably the only infection that is clearly and commonly passed from cat to man. Simple sanitary measures such as keeping pets off the table and washing the hands after handling a cat eliminate most possible risks.
Cats may be poisoned by a variety of substances. They may eat poisonous plants—which include rhododendron, hyacinth, poinsettia, and ivy. Waxes, cleaning fluids, disinfectants, detergents, and mothballs may be toxic or irritating. Antifreeze, weed killers, insecticides, and rodent poisons are outdoor hazards. Cats react adversely to many chemicals and drugs, such as aspirin or iodine, that are safe for humans or other animals. They should never be given medicines not labeled safe for cats or prescribed by a veterinarian.
Bacillary dysentery
(or shigellosis), an infectious disease of the digestive system. Its symptoms are diarrhea, fever, stomach pain, and vomiting. It is transmitted by the Shigella bacterium in contaminated food and water. The incubation period is from one to seven days. The disease is treated by drinking plenty of fluids and taking antibiotics, and preventive measures include improved sanitation and food-handling methods,
Lyme disease
tick-borne microbial disease first recognized in 1975 in Lyme, Conn. In that year two children in Lyme developed swollen and painful joints and were diagnosed as having juvenile rheumatoid arthritis. Their parents learned that many other children and adults in the area had been diagnosed with the same disease. Because rheumatoid arthritis does not usually manifest itself in clusters, the parents informed researchers at Yale University in New Haven, Conn., of the developing problem.
Ticks and Spirochetes
By the late 1970s researchers had traced the cause to a microorganism transmitted by the deer tick Ixodes dammini (now called I. scapularis), which is common in the wooded and grassy areas of Lyme, Conn. In 1982 the actual bacterium responsible for the disease was identified and named Borrelia burgdorferi, after Willy Burgdorfer of Rocky Mountain Laboratories in Hamilton, Mont., who isolated the spirochete, or spiral-shaped organism.
The disease has been identified in other continents of the world including Africa, Asia, Australia, and Europe. In the United States the disease occurs most often in the Northeast, Minnesota, and northern California. Between 15 and 30 percent of all I. scapularis ticks in the larval and nymph stages in the northeastern United States are infected with the B. burgdorferi microbe. About 50 percent of the adult ticks are infected. Between 1 and 3 percent of people in the Northeast who are bitten by an infected tick go on to develop Lyme disease. In northern California the bacterium is carried by the tick I. pacificus. The incidence of human infection with Lyme disease in California is much lower than that in the Northeast because the I. pacificus tick feeds more often on lizards and other animals that are more resistant to infection with the B. burgdorferi microbes.
I. scapularis ticks have a two-year life cycle that includes three feeding sessions. In the first summer, larva may feed on a bird, or on an infected or uninfected mouse. The following spring a nymph that fed as a larva on an infected mouse may feed on a bird, mouse, dog, or human, often transmitting the infection. In the fall an infected adult tick may feed on a deer, horse, dog or human, likewise transmitting the infection. Because the B. burgdorferi microbes are kept alive in part of the mouse population, tick larva become infected each summer if they feed on an infected mouse, thus continuing the cycle.
Course of the Disease
A person may contract the disease when an infected tick, usually in the nymph stage of development, attaches itself to the person's skin and stays attached for 36 to 48 hours. It takes that long for the B. burgdorferi microbes to start to multiply in the tick's gut and travel to its salivary glands. The microbes then have the opportunity to travel with the tick's saliva into the human host. Blood tests can be used to diagnose Lyme disease because human hosts begin to produce antibodies to fight the microbes; however, the antibodies are slow to appear, taking weeks or months after infection to reach detectable levels. Most cases of Lyme disease are easily treated by means of antibiotics if begun early enough. In about 10 percent of infected people who go untreated, the disease may progress to a chronic stage.
Of those who become infected, most will experience at least one symptom. Three to 30 days after the infection begins, most people will develop a round red rash at or near the site of the bite. The rash may expand to several inches in diameter, but it does not hurt or itch. As it expands it tends to clear up in the center so that it resembles a bull's-eye. Even without medical treatment the rash usually disappears within days or weeks, but this does not mean that the disease is cured.
Other symptoms may also occur in the early stages of the disease. These include the influenza-like symptoms of headaches, fatigue, chills, fever, loss of appetite, and backaches. There may also be some joint and muscle pain but no swelling. About one fifth of untreated sufferers may experience neurological symptoms. These can include Bell's palsy, meningitis, encephalitis, and radiculoneuropathy. The temporomandibular joint may also be affected.
These symptoms usually subside even without treatment; however, approximately six months after the tick bite, about half of the people who receive no antibiotics will develop attacks of arthritis with swelling and pain in one or more joints, especially in the knee joint.
The chronic arthritis of Lyme disease is characterized by repeated swelling of one or more joints, which may remain swollen and painful for more than a year. In most other types of arthritis, paired joints on each side of the body are affected. The affected joints of a person suffering from Lyme disease, however, typically are asymmetrical, or unpaired.
The chronic arthritic form of the disease is rare in Europe; however, chronic skin and nervous disorders have been observed. Neurological problems include reduced cognitive ability and insanity. About 10 percent of Europeans who remain untreated go on to suffer a chronic skin disorder in which an area of the skin becomes extremely thin, wrinkled, and red. Untreated infections of B. burgdorferi can cause disorders in nearly every organ, though symptoms involving the joints, nervous system, skin, and heart are the most common. The differing symptoms found in the United States and Europe probably result from different strains of B. burgdorferi.
Mice, Moths, and Acorns
The results of a three-year study published in 1998 revealed that a chain of intricately woven relationships among forest species may control the incidence of Lyme disease. Ecologists studying the relationships among white-footed mice, gypsy moths, and acorns in eastern United States forests found that large crops of acorns support a massive increase in the white-footed mice population. By feeding on gypsy moth larvae, the mice protect oak trees, which then produce more acorns. Although the increased mouse population affords protection to oak trees, however, it also harbors increased numbers of the ticks that spread Lyme disease. This phenomenon is termed a self-perpetuating tiered relationship among species.
The overall abundance of acorns in a given year directly affects the population size of white-footed mice. The increased amount of acorns leads to a population explosion among the mice, who will also feed on gypsy moth larvae and pupae. Gypsy moths usually feed on the leaves of oaks, thereby causing much damage to the trees. By feeding on gypsy moth larvae and pupae, the mice exert an indirect positive effect on the oaks. During years of low or zero acorn production, white-footed mice populations decrease in size; this allows the gypsy moth population to thrive and to forage on oaks.
However, the periodic acorn masts—the seasons when oaks bear acorns, usually two to five years apart—also attract white-tailed deer. The deer serve as hosts to the ticks that carry the spirochete organism that transmits Lyme disease. White-footed mice are also known to serve as hosts for these ticks. This suggests that the periodic masting of acorns in eastern United States forests might indirectly determine the incidence of Lyme disease during mast years, and gypsy moth outbreaks in non-mast years.
By rigorously testing several hypotheses, ecologists out to tease apart the intricacies of the tangled web. First they trapped and removed white-footed mice from several experimental plots to demonstrate that decreased numbers of white-footed mice would result in increased survival of gypsy moth larvae. They then simulated an acorn mast by distributing more than 3 tons of acorns over the plots that had the decreased mouse populations. Mouse numbers increased greatly and gypsy moth populations showed drastically decreased survivorship. The studies conclusively demonstrated that gypsy moth population size depends on the relationship between white-footed mice and acorns.
The researchers also tracked the numbers of ticks and tick larvae during the experiments. White-footed mice are a known reservoir of Lyme disease—this means that the mice carry the ticks that carry the organism that causes the disease, but the mice are not affected by the organism. The researchers found eight times as many tick larvae in the acorn-enriched plots as in the control plots (plots that had the same numbers of mice but were not given acorns). The increased incidence of tick larvae was related to increased numbers of white-tailed deer that were also attracted by the simulated acorn mast. Deer also harbor the ticks that carry Lyme disease. The deer undoubtedly brought increased numbers of adult ticks into the area. Once in the area, the adult ticks could produce large numbers of larvae, which would eventually mature and infest the mice.
The results of the study strongly suggest that increased acorn production directly supports the increased abundance of white-footed mice and deer; an increased population of mice suppresses gypsy moth outbreaks; and mice and deer support tick populations, potentially increasing the risk of Lyme disease. Epidemiologists caution that the study itself does not have much predictive value because of the many other factors important in determining outbreaks of Lyme disease. Ecologists note that the results emphasize the importance of ecosystem management. Attempts to decrease the spread of Lyme disease by trapping white-footed mice would send gypsy moth populations soaring, which would ultimately result in the devastation of the oak population.
Ticks and Spirochetes
By the late 1970s researchers had traced the cause to a microorganism transmitted by the deer tick Ixodes dammini (now called I. scapularis), which is common in the wooded and grassy areas of Lyme, Conn. In 1982 the actual bacterium responsible for the disease was identified and named Borrelia burgdorferi, after Willy Burgdorfer of Rocky Mountain Laboratories in Hamilton, Mont., who isolated the spirochete, or spiral-shaped organism.
The disease has been identified in other continents of the world including Africa, Asia, Australia, and Europe. In the United States the disease occurs most often in the Northeast, Minnesota, and northern California. Between 15 and 30 percent of all I. scapularis ticks in the larval and nymph stages in the northeastern United States are infected with the B. burgdorferi microbe. About 50 percent of the adult ticks are infected. Between 1 and 3 percent of people in the Northeast who are bitten by an infected tick go on to develop Lyme disease. In northern California the bacterium is carried by the tick I. pacificus. The incidence of human infection with Lyme disease in California is much lower than that in the Northeast because the I. pacificus tick feeds more often on lizards and other animals that are more resistant to infection with the B. burgdorferi microbes.
I. scapularis ticks have a two-year life cycle that includes three feeding sessions. In the first summer, larva may feed on a bird, or on an infected or uninfected mouse. The following spring a nymph that fed as a larva on an infected mouse may feed on a bird, mouse, dog, or human, often transmitting the infection. In the fall an infected adult tick may feed on a deer, horse, dog or human, likewise transmitting the infection. Because the B. burgdorferi microbes are kept alive in part of the mouse population, tick larva become infected each summer if they feed on an infected mouse, thus continuing the cycle.
Course of the Disease
A person may contract the disease when an infected tick, usually in the nymph stage of development, attaches itself to the person's skin and stays attached for 36 to 48 hours. It takes that long for the B. burgdorferi microbes to start to multiply in the tick's gut and travel to its salivary glands. The microbes then have the opportunity to travel with the tick's saliva into the human host. Blood tests can be used to diagnose Lyme disease because human hosts begin to produce antibodies to fight the microbes; however, the antibodies are slow to appear, taking weeks or months after infection to reach detectable levels. Most cases of Lyme disease are easily treated by means of antibiotics if begun early enough. In about 10 percent of infected people who go untreated, the disease may progress to a chronic stage.
Of those who become infected, most will experience at least one symptom. Three to 30 days after the infection begins, most people will develop a round red rash at or near the site of the bite. The rash may expand to several inches in diameter, but it does not hurt or itch. As it expands it tends to clear up in the center so that it resembles a bull's-eye. Even without medical treatment the rash usually disappears within days or weeks, but this does not mean that the disease is cured.
Other symptoms may also occur in the early stages of the disease. These include the influenza-like symptoms of headaches, fatigue, chills, fever, loss of appetite, and backaches. There may also be some joint and muscle pain but no swelling. About one fifth of untreated sufferers may experience neurological symptoms. These can include Bell's palsy, meningitis, encephalitis, and radiculoneuropathy. The temporomandibular joint may also be affected.
These symptoms usually subside even without treatment; however, approximately six months after the tick bite, about half of the people who receive no antibiotics will develop attacks of arthritis with swelling and pain in one or more joints, especially in the knee joint.
The chronic arthritis of Lyme disease is characterized by repeated swelling of one or more joints, which may remain swollen and painful for more than a year. In most other types of arthritis, paired joints on each side of the body are affected. The affected joints of a person suffering from Lyme disease, however, typically are asymmetrical, or unpaired.
The chronic arthritic form of the disease is rare in Europe; however, chronic skin and nervous disorders have been observed. Neurological problems include reduced cognitive ability and insanity. About 10 percent of Europeans who remain untreated go on to suffer a chronic skin disorder in which an area of the skin becomes extremely thin, wrinkled, and red. Untreated infections of B. burgdorferi can cause disorders in nearly every organ, though symptoms involving the joints, nervous system, skin, and heart are the most common. The differing symptoms found in the United States and Europe probably result from different strains of B. burgdorferi.
Mice, Moths, and Acorns
The results of a three-year study published in 1998 revealed that a chain of intricately woven relationships among forest species may control the incidence of Lyme disease. Ecologists studying the relationships among white-footed mice, gypsy moths, and acorns in eastern United States forests found that large crops of acorns support a massive increase in the white-footed mice population. By feeding on gypsy moth larvae, the mice protect oak trees, which then produce more acorns. Although the increased mouse population affords protection to oak trees, however, it also harbors increased numbers of the ticks that spread Lyme disease. This phenomenon is termed a self-perpetuating tiered relationship among species.
The overall abundance of acorns in a given year directly affects the population size of white-footed mice. The increased amount of acorns leads to a population explosion among the mice, who will also feed on gypsy moth larvae and pupae. Gypsy moths usually feed on the leaves of oaks, thereby causing much damage to the trees. By feeding on gypsy moth larvae and pupae, the mice exert an indirect positive effect on the oaks. During years of low or zero acorn production, white-footed mice populations decrease in size; this allows the gypsy moth population to thrive and to forage on oaks.
However, the periodic acorn masts—the seasons when oaks bear acorns, usually two to five years apart—also attract white-tailed deer. The deer serve as hosts to the ticks that carry the spirochete organism that transmits Lyme disease. White-footed mice are also known to serve as hosts for these ticks. This suggests that the periodic masting of acorns in eastern United States forests might indirectly determine the incidence of Lyme disease during mast years, and gypsy moth outbreaks in non-mast years.
By rigorously testing several hypotheses, ecologists out to tease apart the intricacies of the tangled web. First they trapped and removed white-footed mice from several experimental plots to demonstrate that decreased numbers of white-footed mice would result in increased survival of gypsy moth larvae. They then simulated an acorn mast by distributing more than 3 tons of acorns over the plots that had the decreased mouse populations. Mouse numbers increased greatly and gypsy moth populations showed drastically decreased survivorship. The studies conclusively demonstrated that gypsy moth population size depends on the relationship between white-footed mice and acorns.
The researchers also tracked the numbers of ticks and tick larvae during the experiments. White-footed mice are a known reservoir of Lyme disease—this means that the mice carry the ticks that carry the organism that causes the disease, but the mice are not affected by the organism. The researchers found eight times as many tick larvae in the acorn-enriched plots as in the control plots (plots that had the same numbers of mice but were not given acorns). The increased incidence of tick larvae was related to increased numbers of white-tailed deer that were also attracted by the simulated acorn mast. Deer also harbor the ticks that carry Lyme disease. The deer undoubtedly brought increased numbers of adult ticks into the area. Once in the area, the adult ticks could produce large numbers of larvae, which would eventually mature and infest the mice.
The results of the study strongly suggest that increased acorn production directly supports the increased abundance of white-footed mice and deer; an increased population of mice suppresses gypsy moth outbreaks; and mice and deer support tick populations, potentially increasing the risk of Lyme disease. Epidemiologists caution that the study itself does not have much predictive value because of the many other factors important in determining outbreaks of Lyme disease. Ecologists note that the results emphasize the importance of ecosystem management. Attempts to decrease the spread of Lyme disease by trapping white-footed mice would send gypsy moth populations soaring, which would ultimately result in the devastation of the oak population.
Mad cow disease
or bovine spongiform encephalopathy (BSE), a neurological disease that primarily affects mature cattle. The first suspected case of BSE occurred in Great Britain in April 1985. A specific diagnosis was arrived at in 1986. By June of 1990 there were 14,324 confirmed cases out of an estimated population of 10 million cattle in Great Britain.
Cases of BSE in British cattle in 1995 totaled more than 146,000. Additional cases were reported in other countries including Switzerland (about 200 cases), Ireland (about 120 cases), and Portugal (about 30 cases). BSE is one of a group of transmissible and fatal spongiform encephalopathies (TSEs) affecting both animals and humans. This has raised concern regarding possible risks to human health. The disease has crossed the species barrier to infect at least 18 other species. Some researchers suggested a possible link between scrapie or BSE and Creutzfeldt-Jakob disease (CJD) in humans.
This suggestion gained more support in 1996 when British scientists reported a series of related findings. A new variant of Creutzfeldt-Jakob disease (nvCJD) was identified as causing a form of CJD that affects younger people. In another finding, the brain proteins most affected by BSE in cows and CJD in humans are much more similar than was previously thought, given the evolutionary distance between the two species. A third report in 1996 announced research showing that not only is nvCJD different from CJD, but also that nvCJD is probably associated with BSE.
Clinical signs of mad cow disease include abnormally stilted gaits, high stepping, heightened sensory perception, itching, anorexia, and excessive licking, ending in death. Abnormal motor nerve control coupled with aggressiveness have earned the disease the common name of mad, or raging, cow disease. Although all types of cattle are susceptible, most cases have been reported in the Holstein-Friesian breed. The first clinical signs, or onset, of the disease has been observed in cattle at an age of 1 year 10 months to 15 years. From onset, the disease course varies from less than 2 weeks to 14 months usually resulting in death or humane destruction within 4 months.
The causative agent of BSE is not known, however, histopathological studies and clinical signs indicate a strong resemblance to that of scrapie, a neurologic disease of sheep. Brain extracts of suspect cattle have produced disease-specific structures known as scrapie-associated fibrils (SAF). SAF are attributed to infectious type agents called prions. Prions are associated with a unique protein found in brain tissue called prion protein (PrP).
In 1979 studies were conducted by the United States Department of Agriculture (USDA) to attempt experimental transmission of scrapie to cattle. Approximately 30 percent of the inoculated cattle developed progressive neurological signs of the disease. Upon initial histological examination scrapie could not be confirmed. However, a more recent examination of the same tissues, coupled with new information, have shown PrP structures to be present.
As of the mid-1990s there was no evidence of animal-to-animal transmission of BSE. BSE is considered a “common source” epidemic, meaning that animals contract the disease from a common element in their environment. Evidence has ruled out such possible sources of the disease as semen, chemicals, inheritance, chemicals, and pharmaceuticals. The primary suspected sources of the disease are diets fed to cattle containing ruminant-based meat and bone protein. Scrapie- or BSE-contaminated carcasses that are rendered for ruminant diets may account for the presence of SAF in the brains of affected cattle. The feeding of animal protein specifically derived from ruminants was ceased in the United Kingdom as of July 1988.
As of 1996, there were no reported cases of BSE in the United States, but scrapie and other forms of spongiform encephalopathy were present, hence the intense interest in BSE. A transmissible form of spongiform encephalopathy found in ranched mink, transmissible mink encephalopathy (TME), in the United States has been primarily attributed to the feeding of scrapie-infected sheep and goat carcasses to minks.
To prevent BSE from entering the United States, USDA's Animal and Plant Health Inspection Service (APHIS) has taken the following steps:
Beginning in July 1989, APHIS banned the importation of live ruminants and ruminant products from countries where BSE is known to exist.
Since 1991, there has been a voluntary ban in place on using products rendered from adult sheep in animal feeds.
In 1986, APHIS established a program for BSE surveillance in the United States and provided specialized training for 250 APHIS veterinarians who conduct field investigations involving animals with any suspicious symptoms.
APHIS veterinary pathologists and field investigators have received training from British counterparts for diagnosing BSE.
More than 60 veterinary diagnostic laboratories throughout the United States are participating in the BSE Surveillance Program, along with the National Veterinary Services Laboratories in Ames, Iowa.
APHIS veterinarians are tracing 499 head of cattle imported from Great Britain between 1981 and 1989 (before the ban on imports went into effect) to check their health status. As of Jan. 22, 1996, no signs of BSE have been found.
Between 1986 and Dec. 31, 1995, approximately 2,660 brain specimens from cattle exhibiting possible neurological problems had been studied by APHIS. All samples submitted were negative.
Cases of BSE in British cattle in 1995 totaled more than 146,000. Additional cases were reported in other countries including Switzerland (about 200 cases), Ireland (about 120 cases), and Portugal (about 30 cases). BSE is one of a group of transmissible and fatal spongiform encephalopathies (TSEs) affecting both animals and humans. This has raised concern regarding possible risks to human health. The disease has crossed the species barrier to infect at least 18 other species. Some researchers suggested a possible link between scrapie or BSE and Creutzfeldt-Jakob disease (CJD) in humans.
This suggestion gained more support in 1996 when British scientists reported a series of related findings. A new variant of Creutzfeldt-Jakob disease (nvCJD) was identified as causing a form of CJD that affects younger people. In another finding, the brain proteins most affected by BSE in cows and CJD in humans are much more similar than was previously thought, given the evolutionary distance between the two species. A third report in 1996 announced research showing that not only is nvCJD different from CJD, but also that nvCJD is probably associated with BSE.
Clinical signs of mad cow disease include abnormally stilted gaits, high stepping, heightened sensory perception, itching, anorexia, and excessive licking, ending in death. Abnormal motor nerve control coupled with aggressiveness have earned the disease the common name of mad, or raging, cow disease. Although all types of cattle are susceptible, most cases have been reported in the Holstein-Friesian breed. The first clinical signs, or onset, of the disease has been observed in cattle at an age of 1 year 10 months to 15 years. From onset, the disease course varies from less than 2 weeks to 14 months usually resulting in death or humane destruction within 4 months.
The causative agent of BSE is not known, however, histopathological studies and clinical signs indicate a strong resemblance to that of scrapie, a neurologic disease of sheep. Brain extracts of suspect cattle have produced disease-specific structures known as scrapie-associated fibrils (SAF). SAF are attributed to infectious type agents called prions. Prions are associated with a unique protein found in brain tissue called prion protein (PrP).
In 1979 studies were conducted by the United States Department of Agriculture (USDA) to attempt experimental transmission of scrapie to cattle. Approximately 30 percent of the inoculated cattle developed progressive neurological signs of the disease. Upon initial histological examination scrapie could not be confirmed. However, a more recent examination of the same tissues, coupled with new information, have shown PrP structures to be present.
As of the mid-1990s there was no evidence of animal-to-animal transmission of BSE. BSE is considered a “common source” epidemic, meaning that animals contract the disease from a common element in their environment. Evidence has ruled out such possible sources of the disease as semen, chemicals, inheritance, chemicals, and pharmaceuticals. The primary suspected sources of the disease are diets fed to cattle containing ruminant-based meat and bone protein. Scrapie- or BSE-contaminated carcasses that are rendered for ruminant diets may account for the presence of SAF in the brains of affected cattle. The feeding of animal protein specifically derived from ruminants was ceased in the United Kingdom as of July 1988.
As of 1996, there were no reported cases of BSE in the United States, but scrapie and other forms of spongiform encephalopathy were present, hence the intense interest in BSE. A transmissible form of spongiform encephalopathy found in ranched mink, transmissible mink encephalopathy (TME), in the United States has been primarily attributed to the feeding of scrapie-infected sheep and goat carcasses to minks.
To prevent BSE from entering the United States, USDA's Animal and Plant Health Inspection Service (APHIS) has taken the following steps:
Beginning in July 1989, APHIS banned the importation of live ruminants and ruminant products from countries where BSE is known to exist.
Since 1991, there has been a voluntary ban in place on using products rendered from adult sheep in animal feeds.
In 1986, APHIS established a program for BSE surveillance in the United States and provided specialized training for 250 APHIS veterinarians who conduct field investigations involving animals with any suspicious symptoms.
APHIS veterinary pathologists and field investigators have received training from British counterparts for diagnosing BSE.
More than 60 veterinary diagnostic laboratories throughout the United States are participating in the BSE Surveillance Program, along with the National Veterinary Services Laboratories in Ames, Iowa.
APHIS veterinarians are tracing 499 head of cattle imported from Great Britain between 1981 and 1989 (before the ban on imports went into effect) to check their health status. As of Jan. 22, 1996, no signs of BSE have been found.
Between 1986 and Dec. 31, 1995, approximately 2,660 brain specimens from cattle exhibiting possible neurological problems had been studied by APHIS. All samples submitted were negative.
Hirschsprung's disease
(or congenital megacolon), a disease characterized by the absence of nerves in the bowel wall. This prevents the normal movement of waste products through the colon, resulting in blockage. In infants, the disease is eventually treated with a colostomy, the removal of the diseased parts of the colon.
Flesh-eating disease
(or necrotizing fasciitis), severe skin infection that causes necrosis, or death, of several layers of the skin. It can be caused by one form of or a combination of rare but extremely virulent strains of bacteria of the genus Streptococcus (group A). Milder forms of these bacteria cause strep throat and scarlet fever. Although these bacteria have probably existed since before the origins of humans, several small but harsh outbreaks of the virulent strains in Europe and North America during the spring and summer of 1994 focused attention on this so-called flesh-eating disease.
Any bacteria can enter the body and eventually the bloodstream through cuts, scrapes, or unhealed sores. Once the virulent strain of Streptococcus is in the bloodstream, it can multiply and quickly spread the infection, which can kill up to one square inch of body tissue per hour. Symptoms, which develop one to three days after exposure, include high fever, blistering of the skin, and muscle soreness. Most people in generally good health are able to withstand the initial infection and never develop the disease. The bacteria are spread only through direct contact with bodily secretions from an infected person. If caught in an early stage, the infection is treatable with antibiotics and replenishment of lost fluids. In severe cases, surgery and amputation may be necessary. About 30 percent of victims eventually die from the disease.
Any bacteria can enter the body and eventually the bloodstream through cuts, scrapes, or unhealed sores. Once the virulent strain of Streptococcus is in the bloodstream, it can multiply and quickly spread the infection, which can kill up to one square inch of body tissue per hour. Symptoms, which develop one to three days after exposure, include high fever, blistering of the skin, and muscle soreness. Most people in generally good health are able to withstand the initial infection and never develop the disease. The bacteria are spread only through direct contact with bodily secretions from an infected person. If caught in an early stage, the infection is treatable with antibiotics and replenishment of lost fluids. In severe cases, surgery and amputation may be necessary. About 30 percent of victims eventually die from the disease.
Catalepsy
a physical state in which muscles of the face, body, and limbs take on a condition of suspended animation; trancelike or unresponsive state of consciousness; also called anochlesia; may last for many hours; body position or expression does not alter and limbs remain in whatever position they are placed (known as flexibilitas cerea, or waxy flexibility); associated with hysteria, epilepsy, and schizophrenia in humans, and with organic nervous disease in animals; may also be caused by brain disease and some drugs.
Leprosy
Throughout the ages leprosy has been one of the most dreaded diseases and its victims the most shunned. Almost all cultures have believed that persons who contracted leprosy were spiritually unclean. In modern times the disease has still retained some of its mythical character, and many people do not realize that leprosy is a disease that is only mildly contagious and not fatal. In the early 1990s the World Health Organization estimated that about 5.5 million people had leprosy.
Cause and symptoms.
Leprosy is caused by a rod-shaped bacterium, Mycobacterium leprae, a relative of the tuberculosis bacillus. The organism was identified in 1874 by Armauer Hansen, a Norwegian physician, and an alternative name for leprosy is Hansen's disease. The infection is very slow to develop, ranging from six months to ten years, and children are much more susceptible than adults.
There are two main types of reaction to M. leprae in the body. In the milder form of the disease, tuberculoid leprosy, the body's cells crowd around the invading organisms in the deep skin layers, which are the first areas of infection. This response sometimes seals off the infection from the rest of the body or at least limits its spread. The reaction, however, destroys hair follicles, sweat glands, and nerve endings at the site of infection. The skin above the site becomes dry and discolored and loses its sense of touch. Fingers and toes that have no feeling are easily injured, and, if the patient has not been trained to take protective measures, they may in time become mutilated and fall off.
In the second and more contagious form of the disease, lepromatous leprosy, the body is not able to mount a resistance, and the M. leprae multiply freely in the skin. Large, soft bumps, or nodules, appear over the body and face. Mucous membranes of the eyes, nose, and throat may be invaded. In extreme cases the voice may change drastically, blindness may occur, or the nose may be destroyed.
Treatment and Research.
Until sulfa drugs were developed in the 1940s and were found to be helpful, there was no satisfactory treatment. Patients were merely isolated in an attempt to protect the larger community, and many victims hid. To avoid the undesirable side effects of sulfa drugs, a group of related drugs known as sulfones was developed. Many patients improve with these drugs, especially those with the tuberculoid form of the disease. In most cases treatment must continue for years. Research was long hampered by scientists' inability to induce leprosy in animals in order to study the disease. In 1960 it was found that M. leprae could be grown on the footpads of mice, but the yield was low. A search then began for an animal with a body temperature similar to that of the mouse footpad and the cooler parts of the human body on which the bacteria thrive. In 1971 it was discovered that leprosy could be established in the nine-banded armadillo and other animals. In 1976 it was found that armadillos get leprosy in the wild.
Cause and symptoms.
Leprosy is caused by a rod-shaped bacterium, Mycobacterium leprae, a relative of the tuberculosis bacillus. The organism was identified in 1874 by Armauer Hansen, a Norwegian physician, and an alternative name for leprosy is Hansen's disease. The infection is very slow to develop, ranging from six months to ten years, and children are much more susceptible than adults.
There are two main types of reaction to M. leprae in the body. In the milder form of the disease, tuberculoid leprosy, the body's cells crowd around the invading organisms in the deep skin layers, which are the first areas of infection. This response sometimes seals off the infection from the rest of the body or at least limits its spread. The reaction, however, destroys hair follicles, sweat glands, and nerve endings at the site of infection. The skin above the site becomes dry and discolored and loses its sense of touch. Fingers and toes that have no feeling are easily injured, and, if the patient has not been trained to take protective measures, they may in time become mutilated and fall off.
In the second and more contagious form of the disease, lepromatous leprosy, the body is not able to mount a resistance, and the M. leprae multiply freely in the skin. Large, soft bumps, or nodules, appear over the body and face. Mucous membranes of the eyes, nose, and throat may be invaded. In extreme cases the voice may change drastically, blindness may occur, or the nose may be destroyed.
Treatment and Research.
Until sulfa drugs were developed in the 1940s and were found to be helpful, there was no satisfactory treatment. Patients were merely isolated in an attempt to protect the larger community, and many victims hid. To avoid the undesirable side effects of sulfa drugs, a group of related drugs known as sulfones was developed. Many patients improve with these drugs, especially those with the tuberculoid form of the disease. In most cases treatment must continue for years. Research was long hampered by scientists' inability to induce leprosy in animals in order to study the disease. In 1960 it was found that M. leprae could be grown on the footpads of mice, but the yield was low. A search then began for an animal with a body temperature similar to that of the mouse footpad and the cooler parts of the human body on which the bacteria thrive. In 1971 it was discovered that leprosy could be established in the nine-banded armadillo and other animals. In 1976 it was found that armadillos get leprosy in the wild.
Coronary Artery Disease
Disease of the coronary arteries that supply oxygen and nutrients to the heart is the most common heart ailment. Coronary artery disease accounts for more than a third of all deaths among males in the United States between the ages of 35 and 55. It also strikes many women past the age of 50. Hypertension (high blood pressure), overweight, cigarette smoking, diabetes mellitus, excess cholesterol, triglycerides and other fats in the blood, and lack of regular exercise contribute to the chance of developing this disease.
Coronary artery disease is characterized by formation of one or more atheromas. These are fatty deposits of cholesterol that form beneath the inner lining of the artery and obstruct the passage of blood needed to nourish the heart muscle. This also sets up conditions for a blood clot in the coronary artery. Atheroma formation seems to run in families. However, eating foods rich in saturated animal fat and cholesterol are also contributing factors.
Many persons with coronary artery disease do not experience any symptoms. However, if the obstruction is bad enough, it may cause angina pectoris, myocardial infarction (heart attack), or heart enlargement and failure. Angina pectoris is a severe, squeezing chest pain that occurs when the coronary blockage prevents adequate oxygen from reaching the heart, especially during periods of exertion. Rest and medication often relieve the pain. Unlike a heart attack, angina is a temporary condition, and heart muscle is not destroyed.
Myocardial infarction is the medical term for a heart attack. When the coronary artery becomes so obstructed that the myocardium, or heart muscle, does not receive oxygen, the muscle tissue dies, or becomes infarcted. For many years doctors believed that the infarction was caused by a blood clot blocking the coronary artery. However, later studies revealed that most clots form in the artery after the infarction.
The first hours after a heart attack are critical because abnormal heart rhythms, or arrhythmias, may develop. Without swift medical intervention, death follows in three or four minutes after an attack. Patients are usually treated in the coronary care unit of a hospital for a few days to enable electronic monitoring of the heart rate and rhythm.
Repeated heart attacks can strain the remaining healthy heart muscle, leading to heart failure. As attacks destroy more and more heart muscle, the remaining muscle enlarges to compensate. Increased pressure in the weakened heart causes fluid to back up into the lungs. As a result, the heart output—that is, the volume of blood pumped out with each contraction—cannot keep pace with the body's oxygen demands.
Coronary artery disease is characterized by formation of one or more atheromas. These are fatty deposits of cholesterol that form beneath the inner lining of the artery and obstruct the passage of blood needed to nourish the heart muscle. This also sets up conditions for a blood clot in the coronary artery. Atheroma formation seems to run in families. However, eating foods rich in saturated animal fat and cholesterol are also contributing factors.
Many persons with coronary artery disease do not experience any symptoms. However, if the obstruction is bad enough, it may cause angina pectoris, myocardial infarction (heart attack), or heart enlargement and failure. Angina pectoris is a severe, squeezing chest pain that occurs when the coronary blockage prevents adequate oxygen from reaching the heart, especially during periods of exertion. Rest and medication often relieve the pain. Unlike a heart attack, angina is a temporary condition, and heart muscle is not destroyed.
Myocardial infarction is the medical term for a heart attack. When the coronary artery becomes so obstructed that the myocardium, or heart muscle, does not receive oxygen, the muscle tissue dies, or becomes infarcted. For many years doctors believed that the infarction was caused by a blood clot blocking the coronary artery. However, later studies revealed that most clots form in the artery after the infarction.
The first hours after a heart attack are critical because abnormal heart rhythms, or arrhythmias, may develop. Without swift medical intervention, death follows in three or four minutes after an attack. Patients are usually treated in the coronary care unit of a hospital for a few days to enable electronic monitoring of the heart rate and rhythm.
Repeated heart attacks can strain the remaining healthy heart muscle, leading to heart failure. As attacks destroy more and more heart muscle, the remaining muscle enlarges to compensate. Increased pressure in the weakened heart causes fluid to back up into the lungs. As a result, the heart output—that is, the volume of blood pumped out with each contraction—cannot keep pace with the body's oxygen demands.
Heart Diseases
Cardiovascular Disease
Cardiovascular disease—disease of the heart or blood vessels—can develop in any part of the circulatory system. Problems can occur with the valves, the sinoatrial node, the heart muscle, or the blood vessels.
Arteriosclerosis
commonly called hardening of the arteries, includes a variety of conditions in which artery walls thicken and lose elasticity. There is evidence that heredity and a high cholesterol level in the blood can lead to atherosclerosis, the most common form of arteriosclerosis. (See also Cholesterol; Food and Nutrition, “Fats and Oils.”)
Hypertension.
The force of the blood being pumped through the arteries exerts pressure on the arterial walls. When this pressure is too high it is an unhealthy condition called hypertension, or, simply, high blood pressure. If left untreated, it can lead to heart attack, stroke, kidney disease, or other illnesses.
Rheumatic fever
causes inflammation of the body tissues, joints, and heart. All heart tissues, including the pericardium, can be affected, but the heart's valves are most often damaged. Antibiotics can lessen the adverse effects and prevent serious heart damage.
Bacterial endocarditis
a bacterial infection of the inner lining of the heart muscle, leads to inflammation of the lining. More than half of the incidents of bacterial endocarditis are a result of rheumatic fever. Bacteria may also be introduced into the bloodstream during minor medical procedures, but this is rare.
Congenital heart disease
is heart disease present at birth. It ranges from minor heart murmurs that require no treatment to fatal structural defects.
Fibrillation.
In a normal, healthy heart the muscles contract and relax in an orderly manner. This rhythmic pulsing can be disturbed, however, by faulty electrical impulses that cause the heart to beat abnormally or irregularly. Ventricular fibrillation—rapid, uncoordinated contractions of the heart—is one of the most serious disturbances of heart rate and rhythm and can lead to cardiac arrest and death. Other rhythm disorders, or arrythmias, include auricular fibrillation and flutter, tachycardia (rapid heartbeat), and bradycardia (slow heartbeat).
Congestive heart failure
occurs when engorgement of the veins serving the lungs or of those serving the rest of the body prevents the heart muscle from being able to pump forcefully enough to deliver an adequate supply of blood to the body. It can be caused by disease of either the heart muscle or the valves.
Heart attack
occurs when the flow of blood to the heart muscle itself is cut off or so severely impeded as to cause destruction of cardiac tissue. It is a life-threatening episode of heart disease and can result from a blood clot or advanced atherosclerosis in the coronary arteries.
Diagnosis and Treatment
A physician can detect many heart conditions before symptoms become apparent by using an instrument called an electrocardiograph, for example. It detects tiny electrical impulses from the contracting heart and records them on an electrocardiogram, or EKG or ECG. Normal hearts produce characteristic peak-and-valley tracings. These reflect the contractions of the auricles and ventricles. A tracing that varies from this pattern may indicate a disorder.
Heart conditions can also be diagnosed with the aid of various types of X rays, including X-ray films and fluoroscopy, which enable physicians to see the heart in action. More detailed examinations can be made using such techniques as angiocardiography, which tracks the passage of blood through the heart, coronary arteries, and larger vessels; computed tomography (CT), which provides a detailed cross-sectional image of the heart; and magnetic resonance imaging (MRI), which can show images of the heart in many planes.
Treatment of heart conditions may be possible with prescribed drugs that improve blood flow, reduce blood pressure, prevent blood clots from forming or enlarging, increase the heart's pumping ability, or regulate the heartbeat. Frequently prescribed drugs include anticoagulants that prevent unwanted clotting and vasodilators that widen the blood vessels.
Other treatments include pacemaker implantation and cardiac catheterization. A pacemaker is an electronic device that produces rhythmic electrical impulses to regulate the patient's heartbeat. In the process known as cardiac catheterization, physicians insert a catheter, or thin plastic tube, through an artery in the arm or leg to reach the coronary arteries. They then inject special enzymes through the tube to dissolve arterial blood clots. In some cases physicians use a small balloon on the end of the catheter. The balloon is inflated slightly in a narrowed artery to widen it.
Coronary bypass surgery may be necessary to provide a new path for blood flow around a blocked artery. In the most radical surgery the patient may undergo a heart transplant, in which the diseased heart is replaced with a healthy heart from a deceased donor.
Most physicians recommend changes or improvements in personal habits as the best way of avoiding the early onset of some types of heart disease. Some preventive measures include controlling obesity, hypertension, blood cholesterol levels, and diabetes; avoiding smoking; and fostering healthful habits such as good nutrition, exercise, stress management, and regular medical examinations.
Cardiovascular disease—disease of the heart or blood vessels—can develop in any part of the circulatory system. Problems can occur with the valves, the sinoatrial node, the heart muscle, or the blood vessels.
Arteriosclerosis
commonly called hardening of the arteries, includes a variety of conditions in which artery walls thicken and lose elasticity. There is evidence that heredity and a high cholesterol level in the blood can lead to atherosclerosis, the most common form of arteriosclerosis. (See also Cholesterol; Food and Nutrition, “Fats and Oils.”)
Hypertension.
The force of the blood being pumped through the arteries exerts pressure on the arterial walls. When this pressure is too high it is an unhealthy condition called hypertension, or, simply, high blood pressure. If left untreated, it can lead to heart attack, stroke, kidney disease, or other illnesses.
Rheumatic fever
causes inflammation of the body tissues, joints, and heart. All heart tissues, including the pericardium, can be affected, but the heart's valves are most often damaged. Antibiotics can lessen the adverse effects and prevent serious heart damage.
Bacterial endocarditis
a bacterial infection of the inner lining of the heart muscle, leads to inflammation of the lining. More than half of the incidents of bacterial endocarditis are a result of rheumatic fever. Bacteria may also be introduced into the bloodstream during minor medical procedures, but this is rare.
Congenital heart disease
is heart disease present at birth. It ranges from minor heart murmurs that require no treatment to fatal structural defects.
Fibrillation.
In a normal, healthy heart the muscles contract and relax in an orderly manner. This rhythmic pulsing can be disturbed, however, by faulty electrical impulses that cause the heart to beat abnormally or irregularly. Ventricular fibrillation—rapid, uncoordinated contractions of the heart—is one of the most serious disturbances of heart rate and rhythm and can lead to cardiac arrest and death. Other rhythm disorders, or arrythmias, include auricular fibrillation and flutter, tachycardia (rapid heartbeat), and bradycardia (slow heartbeat).
Congestive heart failure
occurs when engorgement of the veins serving the lungs or of those serving the rest of the body prevents the heart muscle from being able to pump forcefully enough to deliver an adequate supply of blood to the body. It can be caused by disease of either the heart muscle or the valves.
Heart attack
occurs when the flow of blood to the heart muscle itself is cut off or so severely impeded as to cause destruction of cardiac tissue. It is a life-threatening episode of heart disease and can result from a blood clot or advanced atherosclerosis in the coronary arteries.
Diagnosis and Treatment
A physician can detect many heart conditions before symptoms become apparent by using an instrument called an electrocardiograph, for example. It detects tiny electrical impulses from the contracting heart and records them on an electrocardiogram, or EKG or ECG. Normal hearts produce characteristic peak-and-valley tracings. These reflect the contractions of the auricles and ventricles. A tracing that varies from this pattern may indicate a disorder.
Heart conditions can also be diagnosed with the aid of various types of X rays, including X-ray films and fluoroscopy, which enable physicians to see the heart in action. More detailed examinations can be made using such techniques as angiocardiography, which tracks the passage of blood through the heart, coronary arteries, and larger vessels; computed tomography (CT), which provides a detailed cross-sectional image of the heart; and magnetic resonance imaging (MRI), which can show images of the heart in many planes.
Treatment of heart conditions may be possible with prescribed drugs that improve blood flow, reduce blood pressure, prevent blood clots from forming or enlarging, increase the heart's pumping ability, or regulate the heartbeat. Frequently prescribed drugs include anticoagulants that prevent unwanted clotting and vasodilators that widen the blood vessels.
Other treatments include pacemaker implantation and cardiac catheterization. A pacemaker is an electronic device that produces rhythmic electrical impulses to regulate the patient's heartbeat. In the process known as cardiac catheterization, physicians insert a catheter, or thin plastic tube, through an artery in the arm or leg to reach the coronary arteries. They then inject special enzymes through the tube to dissolve arterial blood clots. In some cases physicians use a small balloon on the end of the catheter. The balloon is inflated slightly in a narrowed artery to widen it.
Coronary bypass surgery may be necessary to provide a new path for blood flow around a blocked artery. In the most radical surgery the patient may undergo a heart transplant, in which the diseased heart is replaced with a healthy heart from a deceased donor.
Most physicians recommend changes or improvements in personal habits as the best way of avoiding the early onset of some types of heart disease. Some preventive measures include controlling obesity, hypertension, blood cholesterol levels, and diabetes; avoiding smoking; and fostering healthful habits such as good nutrition, exercise, stress management, and regular medical examinations.
Disease in Pigs
Pigs are subject to a number of diseases, and some of them can afflict humans as well. (See also Disease, Human.)
Anthrax is an acute, infectious, often fatal disease affecting all warm-blooded animals. In pigs the symptoms include swelling of the throat, weakness, and high temperature. Anthrax can be largely prevented by immunization.
Brucellosis causes infectious abortion in pigs. Its symptoms are not always evident; blood tests are the only reliable method of diagnosis. No known preventive medicinal agents or cures exist for this disease.
Hog cholera is a highly contagious virus that affects only pigs and is the most serious disease of domestic pigs in North America. The disease is marked by sudden onset, fever, loss of appetite, and weakness, though some pigs may die without showing symptoms. This disease has been largely controlled in most of the United States.
Foot-and-mouth disease , or aftosa, is a disease that affects cloven-hoofed animals. It is characterized by blisters and sores in the mouth and on the skin around the hooves. The disease is widespread in Europe, Asia, Africa, and South America.
Swine flu is an acute respiratory disease caused by the combined infection of a bacterium and a virus and can also affect humans. There is no known treatment.
African swine fever is a highly contagious, usually fatal, viral disease of pigs. Its symptoms and lesions resemble those of hog cholera. There is no known vaccine or treatment.
Leptospirosis is caused by a bacterium that is readily transmitted from one species to another and can affect both livestock and humans. Use of vaccines is an effective preventive measure.
Parasites affect pigs probably more often than any other species of livestock, with the possible exception of sheep. Internal parasites of pigs include large intestinal roundworms, coccidia, nodular worms, stomach worms, trichinae, thread worms, and whipworms. External parasites include hog lice, blowflies, mites, ringworms, and screwworms.
History
Wild pigs existed as far back as 36 million years ago. The hunting of wild pigs by early humans was often depicted in Western European cave and rock paintings dating back thousands of years.
Domestic pigs probably descended from one species—the Eurasian wild boar (Sus scrofa). Domestication of the pig coincided with the formation of the first permanent human settlements. The oldest known sites of pig domestication were established about 8,500 to 9,000 years ago in Iraq, Jordan, and Turkestan. The first domestic pigs in China existed about 6,900 years ago and in Great Britain as early as 2,800 years ago. The Vikings and, later, Spanish and English colonists brought swine to the Americas. Today wild or domestic pigs can be found on every continent except Antarctica.
Anthrax is an acute, infectious, often fatal disease affecting all warm-blooded animals. In pigs the symptoms include swelling of the throat, weakness, and high temperature. Anthrax can be largely prevented by immunization.
Brucellosis causes infectious abortion in pigs. Its symptoms are not always evident; blood tests are the only reliable method of diagnosis. No known preventive medicinal agents or cures exist for this disease.
Hog cholera is a highly contagious virus that affects only pigs and is the most serious disease of domestic pigs in North America. The disease is marked by sudden onset, fever, loss of appetite, and weakness, though some pigs may die without showing symptoms. This disease has been largely controlled in most of the United States.
Foot-and-mouth disease , or aftosa, is a disease that affects cloven-hoofed animals. It is characterized by blisters and sores in the mouth and on the skin around the hooves. The disease is widespread in Europe, Asia, Africa, and South America.
Swine flu is an acute respiratory disease caused by the combined infection of a bacterium and a virus and can also affect humans. There is no known treatment.
African swine fever is a highly contagious, usually fatal, viral disease of pigs. Its symptoms and lesions resemble those of hog cholera. There is no known vaccine or treatment.
Leptospirosis is caused by a bacterium that is readily transmitted from one species to another and can affect both livestock and humans. Use of vaccines is an effective preventive measure.
Parasites affect pigs probably more often than any other species of livestock, with the possible exception of sheep. Internal parasites of pigs include large intestinal roundworms, coccidia, nodular worms, stomach worms, trichinae, thread worms, and whipworms. External parasites include hog lice, blowflies, mites, ringworms, and screwworms.
History
Wild pigs existed as far back as 36 million years ago. The hunting of wild pigs by early humans was often depicted in Western European cave and rock paintings dating back thousands of years.
Domestic pigs probably descended from one species—the Eurasian wild boar (Sus scrofa). Domestication of the pig coincided with the formation of the first permanent human settlements. The oldest known sites of pig domestication were established about 8,500 to 9,000 years ago in Iraq, Jordan, and Turkestan. The first domestic pigs in China existed about 6,900 years ago and in Great Britain as early as 2,800 years ago. The Vikings and, later, Spanish and English colonists brought swine to the Americas. Today wild or domestic pigs can be found on every continent except Antarctica.
Notifiable diseases
medical conditions that must be reported to local health authorities by doctor who diagnoses patients with these conditions; include tuberculosis, hepatitis, malaria, food poisoning, scarlet fever, measles, dysentery, birth defects, cancers, lead poisoning, and anthrax; in case of infectious diseases, enables health officials to take necessary steps to control spread of diseases by isolating victims, improving sanitation, or offering immunization to those not yet affected; also provides valuable statistics on incidence and prevalence of medical conditions; practice first introduced in England and Wales in about 1900.
Heartworm disease
serious disease complex of dogs and cats in the United States and worldwide. Heartworm disease is caused by the parasitic filarial worm Dirofiliaria immitis, the adults of which colonize the right ventricle of the heart and the pulmonary artery. The disease, which is transmitted by mosquitoes, is potentially fatal, but it is also completely preventable by properly testing and medicating animals before they become infected. The disease is endemic in the southeastern United States, though the rate of incidence has risen dramatically across the United States; few states report no cases of heartworm.
In the host animal, adult heartworms live in the right ventricle of the heart, the vena cava, and the pulmonary arteries. The adult female worms produce microscopic larvae called microfilaria, which circulate throughout the bloodstream of the host animal, and are ingested by mosquitoes when the latter feed on the host. In the gut of the mosquito, the microfilaria develop into an infective larval form. When the insect bites an uninfected host animal, the infective larvae are injected into the host's tissue, then migrate to the blood, reaching the heart within about four months; in the heart, the larvae mature into adults during the next two to three months. The females produce microfilaria, which enter the circulation, and the cycle perpetuates when the infested blood is ingested by a mosquito.
In the host, the adult worms cause significant damage to the walls of the heart as well as the blood vessels. The vessels become inflamed, and the ventricle of the heart enlarges, causing the right side of the heart to work harder and resulting in enlargement of the right ventricle. The presence of worms in the ventricle and the pulmonary artery further impede blood flow to the lungs, leading to pulmonary hypertension and pulmonary emboli, or blood clots. If the animal is not treated for the disease, death due to right-sided heart failure is usually inevitable.
The pathogenesis of the disease is similar in dogs and cats, though there are important differences. In the dog, as many as 250 adult worms may be present at one time. This is a considerable number, especially if one takes into consideration the size of the adult worms: females average 11 inches (27 centimeters), and males 7 inches (17 centimeters), in length. The number of worms infecting cats is much lower, usually two to three adult worms per cat. The worms live from five to seven years in dogs, but only one to two years in cats. In dogs, the clinical signs of the disease are usually coughing, respiratory distress (labored breathing) and exercise intolerance. Symptoms of the disease in cats vary considerably. Some cats never show any significant signs, appearing normal one day and suffering acute heart failure the next. Other cats develop a chronic form of the disease, with vomiting and respiratory difficulties as the only clinical signs. Regardless of the clinical signs, the disease is usually more severe in cats and more difficult to detect and treat.
Treatment, though effective, is a challenge. For many years, heartworm disease in dogs was treated with arsenamide, a form of arsenic. This drug, though effective at resolving the disease, had serious side effects, including kidney and liver toxicity. New drugs with a higher margin of safety have been developed to treat heartworm disease in dogs. These adulticides kill the adult worms, which must then be cleared by the body. The risk of post-treatment lung inflammation and blood clots is high, hence the dog must be confined for a month after treatment. Other drugs are given to kill the microfilaria circulating in the dog's blood. In cats, treatment is more difficult. Some cats are able to clear the worms without treatment, though monitoring the animal for complications is essential. Supportive therapy, such as fluids and occasionally steroids, are indicated in some cases. The adulticides used to treat the disease in dogs are very risky to use in treating cats because there is a strong chance that the cat will develop pulmonary emboli after receiving the drugs.
The disease is diagnosed by a blood test that reveals the presence of the microfilaria in the blood. In some cases, no microfilaria are present in the blood though the animal is infected and may have adult worms in the heart. These cases, known as occult infection, may be diagnosed based on clinical history of symptoms and chest x-rays.
Heartworm disease is easily preventable. The animal must first be tested to determine if microfilaria are present in the circulation. This is essential, because if preventive medication is given to an animal that is already infected, the results could be fatal. Once the animal tests negative, a monthly medication is administered. This preventive treatment should begin in early spring and should continue for two months after the mosquito season ends. Because of the increasing prevalence of heartworm in the United States, many veterinarians now recommend preventive treatment year-round; however, a yearly test in the spring is still advisable.
In the host animal, adult heartworms live in the right ventricle of the heart, the vena cava, and the pulmonary arteries. The adult female worms produce microscopic larvae called microfilaria, which circulate throughout the bloodstream of the host animal, and are ingested by mosquitoes when the latter feed on the host. In the gut of the mosquito, the microfilaria develop into an infective larval form. When the insect bites an uninfected host animal, the infective larvae are injected into the host's tissue, then migrate to the blood, reaching the heart within about four months; in the heart, the larvae mature into adults during the next two to three months. The females produce microfilaria, which enter the circulation, and the cycle perpetuates when the infested blood is ingested by a mosquito.
In the host, the adult worms cause significant damage to the walls of the heart as well as the blood vessels. The vessels become inflamed, and the ventricle of the heart enlarges, causing the right side of the heart to work harder and resulting in enlargement of the right ventricle. The presence of worms in the ventricle and the pulmonary artery further impede blood flow to the lungs, leading to pulmonary hypertension and pulmonary emboli, or blood clots. If the animal is not treated for the disease, death due to right-sided heart failure is usually inevitable.
The pathogenesis of the disease is similar in dogs and cats, though there are important differences. In the dog, as many as 250 adult worms may be present at one time. This is a considerable number, especially if one takes into consideration the size of the adult worms: females average 11 inches (27 centimeters), and males 7 inches (17 centimeters), in length. The number of worms infecting cats is much lower, usually two to three adult worms per cat. The worms live from five to seven years in dogs, but only one to two years in cats. In dogs, the clinical signs of the disease are usually coughing, respiratory distress (labored breathing) and exercise intolerance. Symptoms of the disease in cats vary considerably. Some cats never show any significant signs, appearing normal one day and suffering acute heart failure the next. Other cats develop a chronic form of the disease, with vomiting and respiratory difficulties as the only clinical signs. Regardless of the clinical signs, the disease is usually more severe in cats and more difficult to detect and treat.
Treatment, though effective, is a challenge. For many years, heartworm disease in dogs was treated with arsenamide, a form of arsenic. This drug, though effective at resolving the disease, had serious side effects, including kidney and liver toxicity. New drugs with a higher margin of safety have been developed to treat heartworm disease in dogs. These adulticides kill the adult worms, which must then be cleared by the body. The risk of post-treatment lung inflammation and blood clots is high, hence the dog must be confined for a month after treatment. Other drugs are given to kill the microfilaria circulating in the dog's blood. In cats, treatment is more difficult. Some cats are able to clear the worms without treatment, though monitoring the animal for complications is essential. Supportive therapy, such as fluids and occasionally steroids, are indicated in some cases. The adulticides used to treat the disease in dogs are very risky to use in treating cats because there is a strong chance that the cat will develop pulmonary emboli after receiving the drugs.
The disease is diagnosed by a blood test that reveals the presence of the microfilaria in the blood. In some cases, no microfilaria are present in the blood though the animal is infected and may have adult worms in the heart. These cases, known as occult infection, may be diagnosed based on clinical history of symptoms and chest x-rays.
Heartworm disease is easily preventable. The animal must first be tested to determine if microfilaria are present in the circulation. This is essential, because if preventive medication is given to an animal that is already infected, the results could be fatal. Once the animal tests negative, a monthly medication is administered. This preventive treatment should begin in early spring and should continue for two months after the mosquito season ends. Because of the increasing prevalence of heartworm in the United States, many veterinarians now recommend preventive treatment year-round; however, a yearly test in the spring is still advisable.
Fifth disease
a mild but contagious viral disease of children that causes a very characteristic facial rash. The formal name for the disease is erythema infectiosum, which means “infectious redness.” The name fifth disease was applied to the condition because it was the fifth pink-red infectious rash of childhood to be described. The others are scarlet fever, measles, rubella, which is often called German measles, and roseola.
Although persons of any age may contract fifth disease, children attending elementary school are the major group at risk. The virus causing this condition, human parvovirus B19, is spread by exposure to airborne droplets exhaled by an infected person. The disease is seen mainly in the spring months, and often occurs as a small outbreak in a geographically limited region.
More than half of the children who are exposed to fifth disease will contract the illness. After an incubation period ranging from four days to two weeks, an infected child usually has a fever of less than 101° F (38° C), may feel slightly ill or tired, and develops the most characteristic sign of fifth disease: a bright red or rosy rash on both cheeks, making them look as if they have been slapped. In fact, the infection has been called “slapped cheeks disease.” The rash does not itch, and may extend to the upper arms, thighs, and buttocks, where it is more pink than bright red and has a lacy or netlike appearance.
Children usually are no longer ill after five to ten days, but the rash often recurs a number of times over a period of several weeks. It seems to be triggered by exposure to direct sunlight, exercising, or emotional stress. The child may continue in school or day care at this stage because once the rash appears, there is no longer any risk of giving the disease to others. The only treatment for the patient during the acute illness phase is bed rest. Drinking plenty of fluids is also important.
Fifth disease generally is diagnosed from the appearance of the rash. A specific blood test will confirm the diagnosis, but it is not necessary in an otherwise healthy child. In some cases, however, it is hard to distinguish the rash characteristic of fifth disease from that of rubella. A blood test is needed to diagnose rubella. Anyone who contracts fifth disease becomes immune to the virus for many years or possibly for life. In fact, more than half of all adults are immune to parvovirus B19.
Most adults who develop fifth disease have only mildly pink cheeks, and some lack a rash altogether. They do tend to develop joint pain and swelling, especially in the knees, which may last as long as three months.
Fifth disease does pose two special risks. If a pregnant woman is exposed, the virus—which damages red blood cells—can produce severe anemia in the developing fetus. (Anemia is a disorder in which an individual has too few red blood cells.) Out of every ten infants who are infected with fifth disease before birth, about one has this complication, which in rare cases proves fatal. The fetus also may develop edema, or swelling, from fluid accumulating in the tissues. There is some indication that exposure to the virus increases the chance of a miscarriage. However, the virus does not cause birth defects, as occur in babies whose mothers had rubella in early pregnancy. The other risk is that some persons with chronic disorders of the red blood cells, such as sickle-cell anemia, may become severely anemic if they contract fifth disease. In patients with a weak immune system, the infection may last much longer than usual and cause marked anemia.
Although persons of any age may contract fifth disease, children attending elementary school are the major group at risk. The virus causing this condition, human parvovirus B19, is spread by exposure to airborne droplets exhaled by an infected person. The disease is seen mainly in the spring months, and often occurs as a small outbreak in a geographically limited region.
More than half of the children who are exposed to fifth disease will contract the illness. After an incubation period ranging from four days to two weeks, an infected child usually has a fever of less than 101° F (38° C), may feel slightly ill or tired, and develops the most characteristic sign of fifth disease: a bright red or rosy rash on both cheeks, making them look as if they have been slapped. In fact, the infection has been called “slapped cheeks disease.” The rash does not itch, and may extend to the upper arms, thighs, and buttocks, where it is more pink than bright red and has a lacy or netlike appearance.
Children usually are no longer ill after five to ten days, but the rash often recurs a number of times over a period of several weeks. It seems to be triggered by exposure to direct sunlight, exercising, or emotional stress. The child may continue in school or day care at this stage because once the rash appears, there is no longer any risk of giving the disease to others. The only treatment for the patient during the acute illness phase is bed rest. Drinking plenty of fluids is also important.
Fifth disease generally is diagnosed from the appearance of the rash. A specific blood test will confirm the diagnosis, but it is not necessary in an otherwise healthy child. In some cases, however, it is hard to distinguish the rash characteristic of fifth disease from that of rubella. A blood test is needed to diagnose rubella. Anyone who contracts fifth disease becomes immune to the virus for many years or possibly for life. In fact, more than half of all adults are immune to parvovirus B19.
Most adults who develop fifth disease have only mildly pink cheeks, and some lack a rash altogether. They do tend to develop joint pain and swelling, especially in the knees, which may last as long as three months.
Fifth disease does pose two special risks. If a pregnant woman is exposed, the virus—which damages red blood cells—can produce severe anemia in the developing fetus. (Anemia is a disorder in which an individual has too few red blood cells.) Out of every ten infants who are infected with fifth disease before birth, about one has this complication, which in rare cases proves fatal. The fetus also may develop edema, or swelling, from fluid accumulating in the tissues. There is some indication that exposure to the virus increases the chance of a miscarriage. However, the virus does not cause birth defects, as occur in babies whose mothers had rubella in early pregnancy. The other risk is that some persons with chronic disorders of the red blood cells, such as sickle-cell anemia, may become severely anemic if they contract fifth disease. In patients with a weak immune system, the infection may last much longer than usual and cause marked anemia.
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