Background

Leprosy, also called Hansen's disease, is an infectious disease that is

characterized by disfiguring skin sores and progressive nerve damage.
Armauer Hansen discovered the disease-causing bacteria in 1873.

There are two types of leprosy: tuberculoid and lepromatous. Both

forms cause skin sores and peripheral nerve damage, but lepromatous
is more severe. It causes large, disfiguring lumps and bumps
(nodules) on the skin. Only the lepromatous form is considered
contagious.

Researchers estimate that more than one million people worldwide

have leprosy. It is most common in Asia (especially Nepal and India),
Latin America, and Africa. An estimated 4,000-6,000 Americans have
leprosy. Nearly all cases of leprosy in the United States occur in
patients who emigrated from developing countries. Leprosy is more
common in developing countries because these areas are more likely
to be unsanitary and highly populated.

According to the World Health Organization (WHO), access to

information, diagnostic procedures, and treatment have helped
decrease the prevalence of leprosy worldwide. Since 1985, 113
countries out of the 122 countries where leprosy was a public health
concern have eliminated the disease. Since 2001, the number of new
leprosy cases has decreased by 20% each year.

Individuals can develop leprosy at any age. However, it is most

common among patients who are in their 20s and 30s. The severity of
leprosy does not vary with age.

Individuals can become infected with either form of leprosy after

coming into contact with Mycobacterium leprae when they are
exposed to contaminated soil or armadillos that carry the bacteria.
However, researchers have not discovered exactly how the disease
spreads from person to person. It was initially believed that the
disease was transmitted after physical contact with an infected
individual. However, experts currently believe that the lepromatous
form of leprosy is passed from person to person through expelled
droplets from the mouth and nose of an infected person. Experts
believe that most cases are spread after close, long-term contact with
an infected individual. According to this new theory, individuals who
inhale these droplets may become infected.

Leprosy is not considered a highly contagious illness. About 95% of

people who are exposed to the bacteria that causes leprosy do not
develop the disease. Healthcare workers often treat people with
leprosy for many years without contracting the disease.

A combination of medications, called antibiotics, is used to kill the

bacterium that causes leprosy. These medications cure the disease and
prevent it from progressing, but they do not reverse nerve damage or
physical disfiguration. Therefore, it is important to visit a healthcare
provider as soon as symptoms develop.

Causes

General: Leprosy is caused by an infection with a bacterium called

Mycobacterium leprae. Patients may come into contact with this
bacterium when they are exposed to contaminated soil or armadillos
that carry the bacteria. Exposure may occur during gardening, hiking,
or other outdoor activities.

Adults are more likely to become infected with leprosy than children
because they are more likely to be exposed to the bacteria. However,
children are more vulnerable to infections after exposure than adults.

Tuberculoid leprosy: The tuberculoid form of leprosy cannot pass

from person to person. Instead, it can only be transmitted through
direct contact with the bacteria in soil or on armadillos that carry the
bacteria.

Lepromatous leprosy: The lepromatous form, on the other hand,

may be passed from person to person. However, researchers do not
consider the disease to be highly contagious. Most cases of
transmission occur after close, long-term contact with an infected
individual. Individuals are most likely to catch leprosy from someone
else if they live with an infected person. This means it is unlikely that
an individual will develop leprosy after short-term or casual contact
with an infected individual. Contrary to popular belief, leprosy cannot
be spread after touching someone who has the disease.

Other possible causes: It has also been suggested, but not proven,
that leprosy may be transmitted through insects, such as mosquitoes
or bedbugs. Further research is needed in this area.

Signs And Symptoms

General: Symptoms of leprosy do not appear for at least one year

after exposure to Mycobacterium leprae. In most patients, it takes five
to seven years for symptoms to develop. This is because the disease-
causing bacteria multiply very slowly. Once symptoms do develop,
they slowly worsen over a long period of time.

Tuberculoid leprosy: Tuberculoid leprosy causes a rash, consisting

of one or more flat, whitish areas on the skin. Areas that are affected
are usually numb because the bacterium damages the
peripheral nerves, which allow patients to feel sensations such as pain
and temperature.

Lepromatous leprosy: Lepromatous leprosy is more disfiguring than

tuberculoid leprosy. Lepromatous leprosy typically causes many
small bumps (called nodules) or raised rashes on the skin. Symptoms
of numbness and muscle weakness are generally much worse in
patients who have lepromatous leprosy than patients who have
tuberculoid leprosy. As a result of this decreased sensation, patients
with lepromatous leprosy often develop blisters and skin wounds on
the soles of the feet. Because patients cannot feel pain, these wounds
often go unnoticed and eventually progress to disfiguring sores and
eruptions.

Complications

General: Medical complications may occur with either type of

leprosy. However, complications are more common and usually more
severe in patients with the lepromatous form of leprosy.
Deformities: Leprosy may cause swelling and bumps or lumps
(nodules) to form on the skin, which may be disfiguring, especially
when the face is affected.

Nerve damage may cause muscle weakness, which may also lead to
deformities. When the muscles become weak, the fingers may have a
claw-like appearance, and the patient may have what is called a
"drop-foot deformity." This means the patient is unable to flex the
foot.

Eye damage: Leprosy may damage the nerves surrounding the eyes.
As a result, the eyes are unable to blink properly. If blinking is
impaired, the eyes become dry and may also become infected. If left
untreated, permanent eye damage or blindness may result.

Erectile dysfunction (ED)/infertility: Males with leprosy may

develop erectile dysfunction (ED). This means the patient is unable to
achieve or maintain an erection. Some men may also become infertile
because leprosy may reduce the amount of testosterone and sperm
that is produced by the testes.

Women do not experience infertility as a result of leprosy.

Inflammation: Leprosy may trigger the immune system to launch an

attack against the disease-causing bacteria. This response may lead to
inflammation in many parts of the body, including the skin, peripheral
nerves, eyes, and sometimes, the lymph nodes, joints, kidneys, liver,
eyes, and testes. Severe inflammation may permanently damage the
affected organs and lead to conditions such as erectile dysfunction.
Patients may also develop fevers.

Nasal passageway: If left untreated, leprosy may damage the nasal

passages. Patients may experience a chronically stuffy nose and
decreased quality of life. Without treatment, the inside of the nose
may become damaged and scarred. In rare cases, this may lead to
complete collapse of the nose.

Nerve damage: Patients who do not receive prompt treatment may

suffer from permanent peripheral nerve damage. When the peripheral
nerves are damaged, a patient's ability to feel sensations, including
pain and temperature, are decreased. As a result, patients have an
increased risk of unknowingly hurting themselves. They may burn or
cut the skin without realizing the severity of the condition because
they have minimal or no feeling in some areas of the body.

Patients may also develop sores that can potentially become infected.
If a severe infection develops, the affected part of the body (most
commonly the feet) may need to be surgically amputated.

Nerve damage may also lead to muscle weakness in the affected areas
of the body.

Diagnosis

A skin scraping test is used to diagnose leprosy. During the

procedure, a small sample of skin cells are removed from an area of
affected skin. The sample is then analyzed in a laboratory. If the
Mycobacterium leprae is present, the patient has leprosy.

Once leprosy is diagnosed, a lepromin skin test can be used to

distinguish between tuberculoid and lepromatous leprosy. During the
procedure, an extract of inactivated leprosy-causing bacteria is
injected under the patient's skin. The healthcare provider observes the
injection site three days and 28 days after the injection. Patients with
tuberculoid leprosy will develop red and swollen skin at the injection
site, indicating a positive reaction to the test. This is because the
immune systems of patients with tuberculoid leprosy react differently
to the antigen.

Treatment

Medications, called antibiotics, are used to kill the bacterium that

causes leprosy. These medications cure leprosy and stop the disease
from progressing, but they do not reverse nerve damage or
disfiguration that has already occurred.
Patients should tell their healthcare providers if they are taking any
other drugs (prescription or over-the-counter), herbs, or supplements
because they may interact with treatment.

Antibiotics: Patients with either type of leprosy receive a

combination of antibiotics, called multidrug therapy (MDT). The
standard combination is dapsone, rifampin (Rifadin® or
Rimactane®), and clofazimine (Lamprene®). A combination of
medication is used in order to prevent the bacteria from becoming
resistant to the drugs. Dapsone usually does not cause serious side
effects. Rifampin is a stronger drug that may cause more serious side
effects that may lead to liver damage. Symptoms of liver damage may
include yellowing of the skin or eyes (jaundice) or fatigue.

Other antibiotics have also been used to treat leprosy. Examples

include ethionamide (Trecator-SC®), minocycline (Dynacin®,
Minocin®, or Myrac®), clarithromycin (Biaxin®), and ofloxacin
(Floxin®).

Reconstructive surgery: Patients with leprosy may develop sores on

their heels, which in severe cases, may lead to decreased tissue on the
feet. In some cases, tissue from other parts of the body may be
surgically removed from one part of the body, such as the leg, and
transplanted to the heels.

Some patients with leprosy may develop a collapsed nose. This

happens when the infection damages the cartilage of the nose. In such
cases, surgery may be performed to reconstruct the nose.

Patients should discuss the potential health benefits and risks of

surgery before making decisions about medical treatments.

Integrative Therapies

Unclear or conflicting scientific evidence:

Zinc: Zinc formulations have been used since ancient Egyptian times
to enhance wound healing. A few studies have examined the efficacy
of zinc treatment in leprosy. Studies of zinc taken by mouth report
positive results, while one study of topical zinc reports negative
results. Further research is needed before a conclusion can be drawn.

Zinc is generally considered safe when taken at the recommended

dosages. Avoid zinc chloride since studies have not been done on its
safety or effectiveness. While zinc appears safe during pregnancy in
amounts lower than the established upper intake level, caution should
be used since studies cannot rule out the possibility of harm to the
fetus.

Traditional or theoretical uses lacking sufficient evidence:

Acacia: The name "acacia" comes from the Greek word akis, which
means "sharp point." When this name was coined, the only known
species of acacias were sharp thorny shrubs and trees of tropical
Africa and Western Asia. Early laboratory studies warrant additional
research into the effects of acacia on leprosy. Currently, it remains
unknown if this is a safe and effective treatment for leprosy.

Acacia is generally considered safe when taken in the amounts

typically found in foods. Avoid if allergic to acacia, pollen, or any
members of the Fabaceae or Leguminosae family. Use cautiously if
taking amoxicillin or iron. Use cautiously with gastrointestinal
disorders, respiratory disorders, or pinkeye. Acacia may prevent the
body from absorbing drugs, and tannins from acacia may increase the
risk of certain cancers. Avoid if pregnant or breastfeeding.

Hops: The hop is a climbing plant native to Europe, Asia, and North
America. The cone-like, fruiting bodies of the plant are most
commonly used as a flavoring agent in beer. It has been suggested,
but not scientifically proven, that hops may help treat leprosy.

Avoid if allergic to hops pollen, peanut, chestnut, or banana. Use

cautiously with a history of breast cancer, uterine cancer, cervical
cancer, prostate cancer, or endometriosis. Use cautiously while
driving or operating heavy machinery. Use cautiously with a history
of diabetes, stomach ulcers, seizures, or asthma. Hops may affect
hormone levels (such as estrogen levels). Dust from hops may contain
harmful bacteria. Avoid if pregnant or breastfeeding.
Omega-3 fatty acids: Omega-3 fatty acids are found in fish oil and
certain plant/nut oils. Fish oil contains both docosahexaenoic acid
(DHA) and eicosapentaenoic acid (EPA). Although it has been
suggested that omega-3 fatty acid may help treat symptoms of
leprosy, studies are lacking in this area. Until well-designed studies
are performed, it remains unknown if this is a safe and effective
therapy for humans.

Omega-3 fatty acid is generally considered safe if taken in doses that

do not exceed the recommended dietary allowance (RDA). Avoid if
allergic to fish, omega-3 fatty acid products that come from fish, nuts,
linolenic acid, or omega-3 fatty acid products that come from nuts.
Avoid during active bleeding. Use cautiously with bleeding disorders,
diabetes, low blood pressure, or if taking drugs, herbs, or supplements
that treat any such conditions. Use cautiously before surgery.

Prevention

Individuals should avoid close, long-term contact with others who

have lepromatous leprosy.

Patients should also avoid touching armadillos because some carry

Mycobacterium leprae. For this reason, individuals should also avoid
eating undercooked armadillo.

Patients who have symptoms of leprosy should seek prompt medical

treatment. Quick diagnosis and treatment helps reduce the risk of
permanent nerve damage and physical disfiguration.

rabies

Rabies infections in people are rare in the United

States. However, worldwide about 50,000 people die
from rabies each year, mostly in developing countries
where programs for vaccinating dogs against rabies
don't exist. But the good news is that problems can be
prevented if the exposed person receives treatment
before symptoms of the infection develop.

Rabies is a virus that in the U.S. is usually transmitted

by a bite from a wild infected animal, such as a bat,
raccoon, skunk, or fox. If a bite from a rabid animal
goes untreated and an infection develops, it is almost
always fatal.

If you suspect that your child has been bitten by a

rabid animal, go to the emergency department
immediately. Any animal bites — even those that don't
involve rabies — can lead to infections and other
medical problems. As a precaution, call your doctor any
time your child has been bitten.

Transmission
About 7,000 cases of rabies in animals are reported
each year to the Centers for Disease Control and
Prevention (CDC). Raccoons are the most common
carriers of rabies in the United States, but bats are
most likely to infect people. Almost three quarters of
rabies cases between 1990 and 2001 came from
contact with bats.

Skunks and foxes also can be infected with rabies, and

a few cases have been reported in wolves, coyotes,
bobcats, and ferrets. Small rodents such as hamsters,
squirrels, chipmunks, mice, and rabbits are very rarely
infected with the virus.

Because of widespread vaccination programs in the

United States, transmission from dogs to people is very
rare. Outside the United States, exposure to rabid dogs
is the most common cause of transmission to humans.

An infected animal has the rabies virus in its saliva and

can transmit it to a person through biting. In rarer
cases, an animal can spread the virus when its saliva
comes in contact with a person's mucous membranes
(moist skin surfaces, like the mouth or inner eyelids) or
broken skin such as a cut, scratch, bruise, or open
wound.

After a bite, the rabies virus can spread into

surrounding muscle, then travel up nearby nerves to
the brain. Once the virus reaches the brain, the
infection is fatal in almost all cases

Signs and Symptoms

The first symptoms can appear from a few days to
more than a year after the bite occurs.

One of the most distinctive signs of a rabies infection is

a tingling or twitching sensation around the area of the
animal bite. It is often accompanied by a fever,
headache, muscle aches, loss of appetite, nausea, and
fatigue.

As the infection progresses, someone infected with

rabies may develop any of these symptoms:

 irritability
 excessive movements or agitation
 confusion
 hallucinations
 aggressiveness
 bizarre or abnormal thoughts
  muscle spasms
 abnormal postures
 seizures (convulsions)
 weakness or paralysis (when a person cannot
move some part of the body)
 extreme sensitivity to bright lights, sounds, or
touch
 increased production of saliva or tears
 difficulty speaking

In the advanced stage of the infection, as it spreads to

other parts of the nervous system, these symptoms
may develop:

 double vision
 problems moving facial muscles
 abnormal movements of the diaphragm and
muscles that control breathing
 difficulty swallowing and increased production of
saliva, causing the "foaming at the mouth"
usually associated with a rabies infection

If Your Child Is Bitten by an Animal

If your child has been bitten by an animal, take the
following steps right away:

 Wash the bite area with soap and water for 10

minutes and cover the bite with a clean
bandage.

 Immediately call your doctor and go to a nearby

emergency department. Anyone with a possible
rabies infection must be treated in a hospital.
  Call local animal-control authorities to help find
the animal that caused the bite. The animal
may need to be detained and observed for signs
of rabies.

 If you know the owner of the animal that has

bitten your child, get all the information about
the animal, including vaccination status and the
owner's name and address. Notify your local
health department, particularly if the animal
hasn't been vaccinated.

 If you suspect that your child has been bitten by

an unknown dog, bat, rat, or other animal,
contact your doctor immediately or take your
child to the emergency department.

Treatment
At the hospital, it is likely that the doctor will first clean
the wound thoroughly and make sure that your child's
tetanus immunizations are current.

To keep any potential infection from spreading, the

doctor may decide to start treating your child right
away with shots of human rabies immune globulin to
the wound site and vaccine shots in the arm. This
decision is usually based on the circumstances of the
bite (provoked or unprovoked), the type of animal
(species, wild or domestic), the animal's health history
(vaccinated or not), and the recommendations of local
health authorities.

Prevention
You can reduce the chances that your family is exposed
to rabies. Vaccinate your pets — dogs, cats, and ferrets
can be infected by rabies. Report any stray animals to
your local health authorities or animal-control officer.
Remind kids that animals can be "strangers," too. They
should never touch or feed stray cats or dogs
wandering in the neighborhood or elsewhere.

As a precaution against rabies or any other infections,

call your doctor if:

 your child has been exposed to an animal that

might have rabies, but is too young to describe
the contact with the animal
 your child has been exposed to bats, even if
there is no bite
 you plan to travel abroad and may come into
contact with rabid animals, particularly if you're
traveling to an area where you might not have
access to health care

African trypnomosis
.

Human African trypanosomiasis, sleeping sickness,[1] African

lethargy,[1] or Congo trypanosomiasis[1] is a parasitic disease of
people and animals, caused by protozoa of the species Trypanosoma
brucei and transmitted by the tsetse fly.[2] The disease is endemic in
some regions of sub-Saharan Africa, covering about 36 countries and
60 million people. It is estimated that 50,000 to 70,000 people are
currently infected, the number having declined somewhat in recent
years.[3] It is believed that many cases go unreported. About 48,000
people died of it in 2008.[4] Four major epidemics have occurred in
recent history: one from 1896–1906 primarily in Uganda and the
Congo Basin, two epidemics in 1920 and 1970 in several

African trypanosomiasis symptoms occur in two stages. The first

stage is known as the haemolymphatic phase and is characterized by
fever, headaches, and joint pains, and itching. Invasion of the
circulatory and lymphatic system by the parasites is associated with
severe swelling of lymph nodes, often to tremendous sizes.
Winterbottom's sign, the tell-tale swollen lymph nodes along the back
of the neck, may appear. If left untreated, the disease overcomes the
host's defenses and can cause more extensive damage, broadening
symptoms to include anaemia, endocrine, cardiac, and kidney
disfunctions. The second stage, called the neurological phase, begins
when the parasite invades the central nervous system by passing
through the blood-brain barrier. The term 'sleeping sickness' comes
from the symptoms of the neurological phase. The symptoms include
confusion, reduced coordination, and disruption of the sleep cycle,
with bouts of fatigue punctuated with manic periods leading to
daytime slumber and night-time insomnia[citation needed]. Without
treatment, the disease is invariably fatal, with progressive mental
deterioration leading to coma and death. Damage caused in the
neurological phase can be irreversible.[5]

In addition to the bite of the tsetse fly, the disease can be transmitted
in the following ways:

 Mother to child infection: the trypanosome can sometimes cross

the placenta and infect the fetus.[6]
 Laboratories: accidental infections, for example, through the
handling of blood of an infected person and organ
transplantation, although this is uncommon.
 Blood transfusion
 Sexual contact (might be possible, but happens rarely)[7]
Two alternative strategies have been used in the attempts to reduce
the African trypanosomiases. The primary method focuses on the
eradication of the tsetse fly, which disrupts transmission rates by
reducing the number of flies. Instances of sleeping sickness are being
reduced by the use of the sterile insect technique. The second tactic is
primarily medical or veterinary and tries to reduce spread of the
parasite by monitoring, prophylaxis, treatment, and surveillance to
reduce the number of people/animals that carry the disease[citation needed].

Regular active surveillance, involving detection and prompt treatment

of new infections, and tsetse fly control is the backbone of the
strategy used to control sleeping sickness. Systematic screening of at-
risk communities is the best approach, because case-by-case screening
is not practical in endemic regions. Systematic screening may be in
the form of mobile clinics or fixed screening centres where teams
travel daily to areas of high infection rates. Such screening efforts are
important because early sympotoms are not evident or serious enough
to warrant patients with gambiense disease to seek medical attention,
particularly in very remote areas. Also, diagnosis of the disease is
difficult and health workers may not associate such general symptoms
with trypanosomiasis. Systematic screening allows early-stage disease
to be detected and treated before the disease progresses, and removes
the potential human reservoir.[9] There is a single case report of sexual
transmission of West African sleeping sickness,[10] but this is not
believed to be an important route of transmission.

[edit] Treatment
[edit] First line, first stage

The current standard treatment for first stage (haemolymphatic)

disease is:

 Intravenous or intramuscular pentamidine (for T.b. gambiense);

or
 Intravenous suramin (for T.b. rhodesiense)
The drug Eflornithine — previously used only as an alternative
treatment for sleeping sickness due to its labour-intensive
administration — was found to be safe and effective as a first-line
treatment for the disease in 2008, according to the Science and
Development Network's Sub-Saharan Africa news updates. [1].
Researchers tracked over 1,000 adults and children at a centre in Ibba,
Southern Sudan—the first use of eflornithine on a large scale— and it
was highly effective in treating the issue.

According to a treatment study of Trypanosoma gambiense caused

human African trypanosomiasis, use of eflornithine (DMFO) resulted
in fewer adverse events than treatment with melarsoprol.[11]

[edit] First line, second stage

The current standard treatment for second stage (neurological phase)

disease is:

 Intravenous melarsoprol 2.2 mg/kg daily for 10 consecutive

days.[12]

Alternative first line therapies include:

 Intravenous melarsoprol 0.6 mg/kg on day 1, 1.2 mg/kg IV

melarsoprol on day 2, and 1.2 mg/kg/day IV melarsoprol
combined with oral 7.5 mg/kg nifurtimox twice a day on days 3
to 10;[13] or
 Intravenous eflornithine 50 mg/kg every six hours for 14 days.
[14]

Combination therapy with eflornithine and nifurtimox is safer and

easier than treatment with eflornithine alone, and appears to be
equally or more effective. It has been recommended as first-line
treatment for second stage T. b. gambiensis disease.[15]

[edit] Resistant disease

In areas with melarsoprol resistance or in patients who have relapsed

after melarsoprol monotherapy, the treatment should be:
  melarsoprol and nifurtimox, or
 eflornithine

Trypanosoma brucei is a parasitic protist species that causes African

trypanosomiasis (or sleeping sickness) in humans and nagana in
animals in Africa. There are 3 sub-species of T. brucei: T. b. brucei,
T. b. gambiense and T. b. rhodesiense.

These obligate parasites have two hosts - an insect vector and

mammalian host. Because of the large difference between these hosts
the trypanosome undergoes complex changes during its life cycle to
facilitate its survival in the insect gut and the mammalian
bloodstream. It also features a unique and notable variable surface
glycoprotein (VSG) coat in order to avoid the host's immune system.
There is an urgent need for the development of new drug therapies as
current treatments can prove fatal to the patient as well as the
trypanosomes.

Cryptococcosis

Cryptococcosis is a defining opportunistic infection for AIDS. Other

conditions which pose an increased risk include certain lymphomas
(e.g. Hodgkin's lymphoma), sarcoidosis, and patients on long-term
corticosteroid therapy.

Distribution is worldwide. The prevalence of cryptococcosis has been

increasing over the past 20 years for many reasons, including the
increase in incidence of AIDS and the expanded use of
immunosuppressive drugs.
In humans, C. neoformans causes three types of infections:

 Wound or cutaneous cryptococcosis

 Pulmonary cryptococcosis, and
 Cryptococcal meningitis.

Cryptococcal meningitis (infection of the meninges, the tissue

covering the brain) is believed to result from dissemination of the
fungus from either an observed or unappreciated pulmonary infection.
Cryptococcus gattii causes infections in immunocompetent people
(those having a functioning immune system), but C. neoformans v.
grubii, and v. neoformans usually only cause clinically evident
infections in persons who have some form of defect in their immune
systems (immunocompromised persons). People who have defects in
their cell-mediated immunity, for example, people with AIDS, are
especially susceptible to disseminated cryptococcosis. Cryptococcosis
is often fatal, especially if untreated.

[edit] Diagnosis

Symptoms include fever, fatigue, chest pain, dry cough, swelling of

abdomen, headache, blurred vision and confusion.[1]

Detection of cryptococcal antigen (capsular material) by culture of

CSF, sputum and urine provides definitive diagnosis. Blood cultures
may be positive in heavy infections.

Cryptococcosis can rarely occur in the immunocompetent person

without HIV, when it usually goes undiagnosed. Less than 250 cases
in all are reported in the medical literature, the majority diagnosed
postmortem.[2]

[edit] Treatment

Treatment options in non-AIDS patients who have reduced immune-

system function is not well studied. Intravenous Amphotericin B
combined with oral flucytosine may be effective. Every attempt
should be made to reduce the amount of immunosuppressive
medication until the infection is resolved.
AIDS patients often have a reduced response to Amphotericin B and
flucytosine, therefore after initial treatment as above, oral fluconazole
can be used.[1] The decision on when to start treatment for HIV is not
yet settled, although one small, under-powered trial suggested that
delaying the start of treatment for 10 weeks may be beneficial in
avoiding deaths from Immune reconstitution inflammatory syndrome
(IRIS).[3]

[edit] Veterinary cases

Cryptococcosis is also seen in cats and occasionally dogs. It is the

most common deep fungal disease in cats, usually leading to chronic
infection of the nose and sinuses, and skin ulcers. Cats may develop a
bump over the bridge of the nose from local tissue inflammation. It
can be associated with FeLV infection in cats.[4][5]

Cretuzfeldt

Creutzfeldt–Jakob disease or CJD (pronounced /ˈkrɔɪtsfɛlt

ˈjɑːkoʊb/;[1] is a degenerative neurological disorder (brain disease)
that is incurable and invariably fatal.[2] It is the most common among
the types of transmissible spongiform encephalopathy found in
humans.[3]

The first symptom of CJD is rapidly progressive dementia, leading to

memory loss, personality changes and hallucinations. This is
accompanied by physical problems such as speech impairment, jerky
movements (myoclonus), balance and coordination dysfunction
(ataxia), changes in gait, rigid posture, and seizures. The duration of
the disease varies greatly, but sporadic (non-inherited) CJD can be
fatal within months or even weeks (Johnson, 1998). In some people,
the symptoms can continue for years. In most patients, these
symptoms are followed by involuntary movements and the
appearance of an atypical diagnostic electroencephalogram tracing.

The symptoms of CJD are caused by the progressive death of the

brain's nerve cells, which is associated with the build-up of abnormal
prion proteins. When brain tissue from a CJD patient is examined
under a microscope, many tiny holes can be seen where whole areas
of nerve cells have died. The word "spongiform" in "transmissible
spongiform encephalopathies" refers to the "spongy" appearance of
the brain tissue.

[edit] Cause

Transmissible spongiform encephalopathy diseases are caused by

prions. The diseases are thus sometimes called prion diseases. Other
prion diseases include Gerstmann–Sträussler–Scheinker syndrome
(GSS), fatal familial insomnia (FFI) and kuru in humans, as well as
bovine spongiform encephalopathy (BSE, commonly known as mad
cow disease) in cattle, chronic wasting disease (CWD) in elk and
deer, and scrapie in sheep. Alpers' syndrome in infants is also thought
to be a transmissible spongiform encephalopathy caused by a prion.[9]
[10]

The prion that is believed to cause Creutzfeldt–Jakob exhibits at least

two stable conformations. One, the native state, is water-soluble and
present in healthy cells. As of 2007, its biological function is
presumably in transmembrane transport or signaling. The other
conformational state is very poorly water-soluble and readily forms
protein aggregates.

People can also acquire CJD genetically through a mutation of the

gene that codes for the prion protein (PRNP). This only occurs in 5–
10% of all CJD cases.

The CJD prion is dangerous because it promotes refolding of native

proteins into the diseased state. The number of misfolded protein
molecules will increase exponentially,[citation needed] and the process leads
to a large quantity of insoluble prions in affected cells. This mass of
misfolded proteins disrupts cell function and causes cell death.
Mutations in the gene for the prion protein can cause a misfolding of
the dominantly alpha helical regions into beta pleated sheets. This
change in conformation disables the ability of the protein to undergo
digestion. Once the prion is transmitted, the defective proteins invade
the brain and are produced in a self-sustaining feedback loop, causing
exponential spread of the prion, leading to death within a few months,
although a few patients have lived as long as two years.

Stanley B. Prusiner of University of California, San Francisco

(UCSF) was awarded the Nobel Prize in physiology or medicine in
1997 for his discovery of prions. For more than a decade, Yale
University neuropathologist Laura Manuelidis has been challenging
this explanation for the disease. In January 2007 she and her
colleagues published an article in the Proceedings of the National
Academy of Science and reported that they have found a virus-like
particle (but without finding nucleic acids so far) in less than 10% of
the cells a scrapie-infected cell line and in a mouse cell line infected
by a human CJD agent.[11]

[edit] Transmission

The defective protein can be transmitted by contaminated harvested

human growth hormone (hGH) products, Immunoglobulins (IVIG),
corneal grafts, dural grafts or electrode implants (acquired or
iatrogenic form: iCJD); it can be inherited (hereditary or familial
form: fCJD); or it may appear for the first time in the patient (sporadic
form: sCJD). In the hereditary form, a mutation occurs in the gene for
PrP, PRNP. Ten to fifteen percent of CJD cases are inherited. (CDC)

The disease has also been shown to result from usage of HGH drawn
from the pituitary glands of cadavers who died from Creutzfeldt–
Jakob Disease,[12] though the known incidence of this cause is (as of
April 2004) quite small. The risk of infection through cadaveric HGH
usage in the US only ceased when the medication was withdrawn in
1985.
It is thought that humans can contract the disease by consuming
material from animals infected with the bovine form of the disease.
The only suspected cases to arise thus far have been vCJD, although
there are fears — based on animal studies — that consuming beef or
beef products containing prion particles can also cause the
development of classic CJD. When BSE material infects humans the
resulting disease is known as (new) variant CJD Disease (nvCJD).[10]

Cannibalism has also been implicated as a transmission mechanism

for abnormal prions, causing the disease known as kuru, found
primarily among women and children of the Fore tribe in Papua New
Guinea. While the men of the tribe ate the body of the deceased and
rarely contracted the disease, the women and children, who ate the
less desirable body parts, were 8 times more likely to contract the
disease from infected tissue.

Prions, the infectious agent of CJD, may not be inactivated by means

of routine surgical instrument sterilization procedures. The World
Health Organization and the US Centers for Disease Control and
Prevention recommend that instrumentation used in such cases be
immediately destroyed after use; secondary to destruction, it is
recommended that heat and chemical decontamination be used in
combination to process instruments that come in contact with high-
infectivity tissues. No cases of iatrogenic transmission of CJD have
been reported subsequent to the adoption of current sterilization
procedures, or since 1976.[13][14][15] Copper–hydrogen peroxide has
been suggested as an alternative to the current recommendation of
sodium hydroxide or sodium hypochlorite.[16] Thermal
depolymerization also destroys prions in infected organic and
inorganic matter, since the process dissolves protein at the molecular
level.