Primarily a disease of animals

Human cases reflect animal rabies distribution and the degree of human-animal contact

1. 4,700,000

2. 800,000

1. Typically 30-90 days (extremes are 5 days to > 2 yrs)

2. Virus initially bind to/multiplies in myocytes --> eventually enters sensory or motor axons; moves towards CNS by axoplasmic flow

1. Fever, chills, malaise

2. Generally vague respiratory, GI, or neurologic symptoms

3. Paresthesia at or near bite site

1. The furious form (~80%) of the neurologic stage

2. hallucinations, agitation; thrashing, biting, running; hydrophobia/aerophobia; fluctuating mental status

1. Paralytic form

2. weakness, flaccid paralysis sometimes starting in the bitten extremity; paraplegia, quadriplegia; ascending paralysis

1. Human diploid cell vaccine (HDCV); Imovax Sanofi Pasteur Inc.

2. RabAvert rabies vaccine, also known as Purified Chick Embryo Cell vaccine (PCECV) from Chiron Corporation

Primary series:  Vaccines x 3 IM injection into the deltoid

Periodic serology recommended to determine when booster is required

Does not eliminate the need for post-exposure prophylaxis after a recognized exposure

Immediate cleansing of wound w/soap & water

1. Human rabies immune globulin (HRIG) on day 0

20 IU per kg, infiltrated at wound site to extent possible

give any remaining HRIG IM at site distal from vaccination site

2. Vaccine (HDCV, PCEC, or RVA) x 4 (previously 5)

1 ml into deltoid, days 0,3,7, and 14 (day 28 dose eliminated)

Immediate cleansing of wound w/soap & water

1. Vaccine x 2: 1 ml into deltoid, days 0 and 3

2. Do not use HRIG

1. Presence of infective virus

typically in saliva, but also neural tissue, CSF

contact w/blood, urine, feces does not constitue an exposure per CDC

rabies virus is considered non-infectious in dried material

2. The potentially infectious material must come in contact w/an open wound, scratch, abrasion, or mucosal surface

1. BITE

2. NON-BITE (rare)

potentially infective material in contact w/mucous membrane or break in the skin - consider fomites, scratches

tissue transplants

ingestion

bat "exposures" warrant special consideration

That the vast majority of bat variant-associated human cases had no definite history of a bite (bite/scratch likely went unnoticed)

Recommended that rabies postexposure prophylaxis should be considered when the person has been in close physical proximity to a bat and the person cannot exclude the possibility of a bite or scratch, unless bat is negative upon lab testing (this does not include being in the same room as a bat in a competent awake adult)

True/False:  VHF are not naturally occurring diseases.

Transmitted to humans by infected animals or arthropod vectors

Produce microvascular damage

Nonspecific prodrome (fever, myalgias, headache, abdominal pain, prostration)

Exam may show only flushing of face and chest, conjunctival injection, and petechiae

Disease progresses to shock and generalized mucous membrane hemorrhage

From Vervet monkeys!

A filamentous virus was isolated from them - the first member of the genus Filovirus

Cercopithecine Herpes Virus 1

B Virus

Herpes B

Monkey B virus

Herpes simiae

CHV-1

Simian B disease

Derived from the initials of the first human case of Macacine Herpes Virus 1

A 29 yr-old lab worker ("W.B.") who developed fatal meningoencephalitis and transvere myelitis following a bite on the hand from a seemingly healthy rhesus monkey

Alpha herpesvirus

dsDNA

Enveloped

Icosahedral capsid

Members of the genus Macaca (> 16 species) are natural hosts of the virus; almost all of these species are found in Asia

Infection is particularly enzootic in the rhesus (Macaca mulatta) and cynomolgus (Macaca fascicularis)

Captive - variable but up to 100%

Wild and semi-free-ranging - higher than 70%

Dramatically increased w/age

Horizontal rather than vertical transmission

1. Macaques transmit MHV-1 to each other thru oral, ocular, or genital contact of mucous membranes or lesioned skin

2. Can be shed asymptomatically, including thru bodily fluids (semen, mother's milk, saliva, perhaps even in aerosol form).  Animal stools also could conceivably transmit the B virus

3. For captive macaques, transmission often may occur during routine colony management protocols involving tube sharing, common instrumentation, or contaminated gloves

4. Animals most frequently become infected as juveniles at the onset of sexual activity; however, younger animals can become infected thru contact w/another virus-shedding animal (ex. mother grooming an infant)

They are very similar to those symptoms caused by herpes simplex virus in humans

Most obvious manifestation is fluid-filled vesicles on the back of the tongue, lips, and elsewhere in the mouth; occasionally, the vesicles appear on the skin

When the vesicles rupture, they often give rise to ulcers and fibronecrotic scabs, which may lead to secondary bacterial and fungal infections.  Scabs typically heal w/in 7-14 days

In rare instances.

Will see ulcerative lesions in the mouth, esophagus, and stomach, necrosis of the liver, spleen, and adrenal glands

The virus occurs in monkeys as a latent infection and is reactivated spontaneously, resulting in shedding of virus in saliva; during periods of stress or diminished immuno-competence, higher rates of virus shedding occur

Transmission to humans occurs after a monkey bite or by direct or indirect contact/exposure of naked skin (broken or mucous membranes) to infected saliva, tissues, tissue fluid or monkey cell cultures, or by splashes or droplets of infected fluids to the eyes

There has been one apparent case of this: a woman with dermatitis on her finger

She touched her husband's herpetiform lesion which resulted from a monkey bite (I read this and immediately went dirty-minded ;-) guess I need to get my mind outta the gutter)

1. Since 1932 - 31 documented infections of which 21 were fatal

2. Cases occurred in 1950's and 1960's due to use of rhesus macaques in production and testing of poliomyelitis vaccines.  Also several cases since late 1980s coinciding w/an increased use of macaques in retroviral research

1. Limited availability of MHV-1 diagnostic facilities (i.e. actual cases not identified)

2. Some other factors responsible (e.g. different animal-handling procedures)

Approximately 70%, a rate similar to untreated Herpes Simplex Virus encephalitis.

Occasional recoveries have considerable residual disability

They are variably present

1. Pain or pruritus at exposure site

2. Vesicles or ulcers at or near the exposure site

3. Local lymphadenopathy

They are also variably present

1. Fever

2. Malaise

3. Diffuse myalgias

4. Headache

5. Numbness or paresthesia at or near exposure site

6. Nausea and/or abdominal pain

7. Persistent hiccups

1. Persistent headache

2. Alteration of mentation

3. Focal neurological complaints

Serologic evaluation of the exposed patient

If frozen serum from the last 6 months is not available, acquire, freeze, and store a serum sample.

Obtain a follow-up serum sample approximately 3 wks after exposure or after the onset of illness (as close to 3 wks as possible) to test w/the initial specimen for herpes B virus seroconversion

Cleansing of the exposed area w/in minutes of the episode is the only means of preventing a contaminated wound from progressing to actual infection.  The B virus is likely to enter host cells w/in 5 minutes.

At least 15 minutes of scrubbing and/or irrigating the exposed area is recommended.  Sterile saline or rapidly flowing water is used for the eye, and decontaminants (e.g. soap solution, povidone-iodine, chlorhexidine) can be used at other sites.

1. Skin or mucosal exposure to high-risk source

2. Inadequately cleaned skin or mucosal exposure

3. Laceration of head, neck, or torso

4. Deep puncture bite

5. Needlestick associated w/high-risk tissue/fluid

5. Positive post-cleaning culture

1. Skin exposure in which the sking remains intact

2. Exposure associated w/non-macaque species

Some experts suggest surgical excision of needle-track sites under local anesthesia to reduce exposure and increase contact w/detergent.

Surgery is usually not justified unless it can be done w/in minutes

Since October 10, 1975; nonhuman primates have been prohibited for importation as pets, and neither nonhuman primates imported since that date nor their offspring may be legally bred or distributed for any other uses than bona fide science, university-level educational programs, or full-times zoologic exhibition. 

The maintainence of nonhuman primates as pets, hobby, or an avocation w/occasional display to otherss is not a permissible use.

Captive-bred offspring of animals purported to have been imported before October 10, 1975 are frequently offered for sale.

1. Lymphocytic choriomeningitis virus - Lymphocytic choriomeningitis

2. Lassa virus - Lassa fever

3. Junin virus - Argentine hemorrhagic fever

4. Machupo virus - Bolivian hemorrhagic fever

5. Guanarito virus - Venezuelan hemorrhagic fever

6. Sabia - Brazilian hemorrhagic fever

Host - common house mouse, Mus musculus

Found in the saliva, urine, and feces of infected mice.  Infected mice carry and shed it for the duration of their lives w/o showing any sign of illness

Individuals become infected w/LCMV after exposure to fresh urine, droppings, saliva, or nesting materials.

Transmission can also occur when these materials are directly introduced into broken skin, the nose, the eyes, or the mouth, or presumably, via the bite of an infected rodent

In Europe, the Americas, Australia, and Japan

May occur wherever infected rodent hosts of the virus are found

A characteristic biphasic febrile illness then follows.

The intial phase, which may last as long as a week, typically begins w/any or all of the following symptoms:  fever, malaise, lack of appetite, muscle aches, headache, nausea, and vomiting.

Following a few days of recovery, the second phase of the disease occurs, consistenting of symptoms of meningitis (for example: fever, headache, and a stiff neck) or characteristics of encephalitis (for example: drowsiness, confusion, sensory disturbances, and/or motor abnormalities, such as paralysis)

1. Avoid contact w/house mice and their excretions

2. Although rare, pet rodents may become infected w/LCMV from wild rodents.  Pet rodents should not come into contact w/wild rodents

3. If you have a pet rodent, wash your hands w/soap and water after handling rodents or their cages and bedding

Fever, retrosternal pain, sore throat, back pain, cough, abdominal pain, vomiting, diarrhea, conjunctivitis, facial swelling, proteinuria, and mucosal bleeding.

Neurological problems have also been described, including hearing loss, tremors, and encephalitis

1. Deafness (~33% of cases)

2. Increased maternal mortality in third trimester (>30%)

3. Spontaneous abortion

1. Contagious ecthyma

2. Infectious pustular dermatitis

3. Contagious pustular dermatitis

4. Sheep-pox

5. Lip scab of sheep

6. Sore mouth disease

7. Scabby mouth disease

Widespread in sheep and goats, also found in llamas, alpacas, camels, and reindeer

Affects all breeds of sheep.  Young animals are generally more suceptible than adults

Scabs usually appear about 3-14 days after exposure to the virus

Scabs last 1-6 weeks

Reduced gain and feed efficiency

Most serious when nursing animals contract the disease

Affected lambs/kids refuse to nurse and may die from starvation

Yes may be transmitted to the teats and udder of the mother, causing pain and abdonment of the lamb or kid.

Mastitis may also result

Virus can survive for very long periods in scabs from infected animals that drop into the bedding and environment.  This may serve as a source of infection for other animals (and humans) many months later.

The disease is commonly introduced into a flock/herd by replacement or breeding animals and by contact w/bedding material, trucks, and vehicles contamined by ORF virus.

FALSE!!

No transmission occurs to cattle, and no human-to-human transmission occurs

Appears as a solitary lesion or as a few lesions, usually on the fingers, hands, or forearms

The fully developed lesion is typically 2-3 cm in diameter, but it may reach 5-10 cm.  It is often tender and may bleed easily.

May have regional lymphadenopathy

May have mild fever and malaise

6 stages

Each can last up to a week

1. PCR can definitively identify a parapoxvirus as orf virus

2. Serologic tests and electron microscopy cannot distinguish orf virus from other parapoxviruses such as paravaccinia (pseudocowpox) virus

1. A self-limiting disease

2. Symptomatic treatment w/moist dressings, local antiseptics, and finger immobilization is helpful

3. Secondary bacterial infection should be treated w/topical or systemic antibiotics

Average seasonal flu actually kills more per year than the H1N1 pandemic did in 2009

The age group affected in the average seasonal flu is > 65 while the age group affected with H1N1 is those < 65

1. Fever

2. Cough

3. Sore throat

4. Runny or stuffy nose

5. Body aches

6. Headache

7. Chills

8. Fatigue

9. Vomiting

10. Diarrhea

Type A - infects multiple species

Type B - humans

Type C - humans and swine

Virus type/Type of nuclear protein - Geographic origin - strain number - year of isolation ; virus subtype (hemagglutinin and neuraminidase)

Ex:  A/USSR/90/77 (H1N1)

PB1, PB2, PA - replication

NS₂ (NEP)

M₂ (ion channel) - penetration

Lipid bilayer

HA (hemagglutinin) - attachment, penetration

NA (neuraminidase) - release

M1 (matrix protein) - assembly

NP (nucleocapsid) - RNA transport, replication

Humans

Avian influenza

H1N1 pandemic strain

Hemagglutinin (H or HA)

Neuraminidase (N or NA)

Two strains of type A

One strain of type B

Types A and B

Hemagglutinin and Neuraminidase

Water fowl

H1-H16

N1-N9

Humans, swine, ferrets, dogs, horses, whales

H5 and H7 subtypes include viruses that are highly pathogenic for poultry

TRUE!!

Virulence:  HA, NA, M, PB1, PB2

Host range:  HA, NA, M, PB2

1. Severity of disease

2. How easily transmitted person-to-person

1. Genetic mixing of human and animal viruses (ex: swine and birds co-infected >1 virus - viruses emerge w/different combinations of RNAs)

2. Direct transmission from animal viruses

1. Little or no immunity in population

2. Easily transmitted among human population

3. Higher proportion of deaths in younger adults

1. Camp Fundsten (a.k.a. Fort Reilly - outside of Fulton, Kansas)

2. Called it Spanish b/c didn't want it to be associated w/the US and we were still pissed at the Spanish for their civil war

It killed 3-6% of the world population

It infected 1/4 of world population

Came at the end of WWI

Spanish Influenza (1918)

 Swine Influenza (1977)

Swine (H1N1) Influenza (2009)

1. April 15, 2009

2. June 19, 2009

Highly contagious

Not highly lethal

1. Low pathogenic AI (LPAI) - H1 to H15 subtypes

2. Highly pathogenic AI (HPAI) - some H5 or H7 subtypes

Geese and ducks can carry the virus w/o having symptoms

If chickens and turkeys are allowed to commingle w/wild geese and ducks, they can get the virus and develop disease

Migratory birds can carry the virus long distances

Outbreaks in area farms and live bird markets.

Swine are potentially a mixing vessel

There are some examples of human-human transmission

Risk is low

Strains vary in ability to infect humans

High occupational exposure may increase risk

Toxoplasma gondii

An obligate intracellular protozoan parasite

1. Congenita

2. Ingestion of sporulated oocysts from feces

3. Ingestion of infected intermediate hosts

Prepatent period approximately 3 days

Naive cats will shed oocysts for 7-10 days

Prepatent period > 20 days

Oocyst shedding for several weeks

(Oocysts shedding in chronically infected cats can be induced w/extremely high doses of glucocorticoids)

Oocysts in fresh feces are not infective!  Oocysts must sporulate, a process that takes 1-5 days, depending upon environmental conditions

Infection from direct contact w/oocyst-shedding cats is extremely unlikely due to grooming behavior of cats.  Cats would remove oocysts before they had time to sporulate.

Most common is either via geophagia while working w/soil or by drinking contaminated water.

Eating undercooked meat (pork) or improperly washed fruits and vegetables

Infrequently cleaned, poorly sanitized litter boxes

1. Ocular infections/blindness

2. Hepato and splenomegaly

3. Hydrocephalus

4. Jaundice

5. Mental retardation

6. Cerebral palsy

7. Seizures

8. Miscarriages/stillbirth

In the US, 2-6 per 1,000 pregnant women acquire toxoplasmosis

In the US, 1 baby in 10,000 births will have congenital toxoplasmosis

In France, 1 baby in 1,000 births will have congenital toxoplasmosis

Avoid feeding cats undercooked meats

Do not allow cats to hunt

Clean litter box daily; flush feces or discard in a sealed bag

Wear gloves when working w/soil

Keep children's sandboxes covered

Wash all raw fruits and vegetables

Avoid eating undercooked meats (lamb, pork) - microwaving may not kill cysts

 If you have a cat who is T. gondii seronegative what should you tell the client?

"Creeping eruption"

Ancylostoma caninum

Ancylostoma braziliense

Uncinaria stenocephala - Northern hookworm of dogs

More prevalent in countries w/warm climates

Affects more children than adults

In the US, Southeastern states have the highest rates of infection

When human skin comes into contact w/infested soil, larvae burrow into the skin, causing intense inflammatory response.

Larvae may migrate from a few millimeters to a few centimeters a day

Raised, snakelike tracks in the skin that may migrate over time

Itching at the site of penetration of the larvae and along the migratory path - may be worse at night

Occasional blister formation

Human eosinophilic enterocolitis - rare

Occurs when hookworm larvae migrate systemically to GI tract, causing acute abdominal pain, anorexia, nausea, and diarrhea

Ulceration of terminal ileum and colon w/eosinophilic inflammatory response

NOT preceded by CLM lesions

EDUCATE CLIENTS

Public sanitation - clean up after pets

Deworm all puppies and kittens; check fecals annually on adults

Prescribe heartworm preventative that also control hookworm infection

Wear shoes in endemic areas

Toxocara canis

Toxocara cati

Baylisascaris procyonis

Ascaris suum (not common)

Dead-end hosts - larvae cannot complete their life cycle

However, they can persist in tissue, resulting in an immune-mediated inflammatory response

Nausea

Fever

Myalgia

Hepatosplenomegaly

Edema

Urticaria (hives)

Epilepsy (toddlers)

Eosinophilia and leukocytosis

Death is rare

Leukocoria (white mass in the pupillary region)

Loss of vision in affected eye

Eye pain

Strabismus (crossed eyes)

Unnecessary  enucleation - mistaken for retinoblastoma

VLM - most common in children 1-4 yrs old but can occur at any age

OLM - more common in school-age children

EDUCATE CLIENTS

Deworm dogs and cats

Promptly dispose of animal waste

Minimize exposure of children to areas that may be contaminated w/animal feces

Wash hands after handling soil

Roundworm of raccoons

Life cycle can be direct or can involve a paratenic host

1. Minimize contact w/raccoons - educate clients about dangers of having raccoons as pets, raccoons are scavengers so prevent access to trash or other food sources outside

2. Use appropriate care when removing raccoon feces - extremely resistant to disinfectants, including bleach; flaming may be the only effective method; use protective equipment to prevent inhalation

Certain areas where raccoons prefer to relieve themselves.

Generally on horizontal surfaces, such as downed logs, tree crotches, flat stones, or barn lofts.

Since each defecation can contain millions of eggs, latrines are focal points for infection.

Even after the raccoon manure has rotted away, the eggs may remain - in moist soil, they stay alive for several years

The adult tapeworms reside in the small intestine of the host, where they attach to the intestinal mucosa by their scolex.

They produce proglottids which have two genital pores.  This is helpful for identification as not all tapeworms have two genital pores.

The proglottids mature, become gravid (they're knocked up), detach from the tapeworm, and migrate to the anus or are passed in the stool

The proglottids contain egg packets which they release into the environment

The eggs are then ingested by the intermediate host, a flea.

An onchosphere develops in the flea and is released into its intestine

The oncosphere penetrates the intestinal wall, invades the insect's body cavity, and develops into a cysticercoid.

The flea containing a cysticercoid is infective to the definitive host and if ingested by the vertebrate host can complete its life cycle.

In the small intestine of the vertebrate host the cysticercoid develops into the adult tapeworm which reaches maturity about 1 month after infection.

Diagnosis - based on finding proglottids

Treatment - same as for dogs and cats - praziquantel (brand name Biltricide [Droncit])

Control fleas on pet and in environment

Educate clients to look for tapeworm segments; treat promptly when found

Poop patrol

1. Northern - found in tundra; slyvatic form that parasitized wolves, bison, and cervids (moose, elk, deer, caribou)

2. Southern European - pastoral or domestic form; found in domestic ungulates and dogs; may involve wild canids and other carnivores, wild ungulates, and rarely lagomorphs

9 different strains

Horse and dog cycle (Europe)

Camel and dog cycle (Iran)

Swine and dog (Poland)

Reindeer and dog (Alaska, Scandinavia)

1. Echinococcus multilocularis

2. In North America, predominately in north central region from eastern Montana to central Ohio.  Also Alaska and Canada

Definitive = foxes***, dogs, cats, coyotes, wolves.  Prevalence up to 50% in some regions

Intermediate = rodents

Ingestion of food items contaminated w/feces from definitive hosts.  Could include vegetables, berries, etc.

Petting or handling dogs or cats either infected w/the Echinococcus tapeworm or that may have rolled in the feces of an animal that is infected

Each oncosphere develops into a cyst in the target organ which is most often liver but can be lungs, brain, skeletal muscle, or eye.

Cysts are thick-walled, fluid-filled and 2-30 cm in diameter

Take 1-2 yrs to develop

Liver cysts - obstructive jaundice

Peribronchial cysts - pulmonary abscesses

Renal cysts - renal dysfunction; death

Brain cysts - epilepsy; death

Cyst rupture - anaphylaxis

Clinical symptoms suggestive of slow growing tumor plus eosinophilia

Serology (ELISA) to detect antibodies to cyst fluid or protoscolices

Intradermal (Casoni) test w/cyst fluid (not as reliable as serology)

Radiographs

Autopsy

Surgical removal of cysts

Albendazole to kill any remaining larvae

Not always cured by surgery

Not feasible in wild canids

Domestic canids and cats - regular worming; do not feed carcasses to dogs or cats; rodent control

NO VACCINE AVAILABLE for domestic canids and cats

EG95 vaccine in livestock - kills oncosphere early in infection

Destroy contaminated material by heat; chemical disinfection is not reliable

(first off - this contains the word hymen...what does this disease do???)

Hymenolepiasis is caused by two cestode species Rodentolepis nana (the dwarf tapeworm, adults measuring 15-40 mm in length) and Hymenolepis diminuta (rat tapeworm, adults measuring 20-60 cm in length)

Both tapeworms can be found in mice

Rodentolepis nana and Hymenolepis diminuta can be transmitted by an indirect mode w/cockroaches, grain beetles, or fleas as intermediate hosts.  Rodentolepis nana can also be transmitted by direct ingestion of hexacanth ova or by autoinfection in which the entire life cycle occurs in the host's small intestine (complete life cycle in 14-16 days)

***R. nana has both a direct and indirect life cycle

FALSE!!

They are immediately infective when passed w/the stool and cannot survive more than 10 days in the external environment

When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine

When eggs are ingested (in contaminated food or water or from hands contaminated w/feces) the oncospheres contained in the eggs are released.

The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae

After rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scolices, attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine, producing gravid proglottids.  Eggs are passed in the stool when released from proglottids through the genital atrium or when proglottids disintegrate in the small intestine.

An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle w/o passage thru the external environment.

The life span of adult worms is 4-6 wks but internal autoinfection allows the infection to persist for years

Eggs are passed out in the feces of the infected definitive host (rodents, man).

The mature eggs are ingested by an intermediate host (various arthropod adults or larvae), and oncospheres are released from the eggs and penetrate the intestinal wall of the host, which develop into cysticercoid larvae.

The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood.

H. diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae.  Humans can be accidentally infected thru the ingestion of insects in precooked cereals, or other food items, and directly from the environment (e.g. oral exploration of the environment by children)

After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine.

Eversion of the scolices occurs shortly after the cysticercoid larvae are relased. Using the four suckers on the scolex, the parasite attaches to the small intestine wall.

Maturation of the parasites occurs w/in 20 days and the adult worms can reach an average of 30 cm in length.  Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms.  The eggs are expelled to the environment in the mammalian host's feces.

Visualization of proglottids

Recovery of hexacanth ova in feces

Most ppl who are infected don't have any symptoms

Those who have symptoms may experience nausea, weakness, loss of appetite, diarrhea, and abdominal pain.

Young children, esp. those w/a heavy infection, may develop a headache, itchy perineum, or have difficulty sleeping.

Sometimes infection is misdiagnosed as a pinworm infection

Infection w/dward tapeworm is generally not serious. 

However, prolonged infection can lead to more severe symptoms so medical attention is needed to eliminate the tapeworm

Vermin control:  rodents and intermediate hosts (cockroaches)

Wash hands w/soap and water after using the toilet, and before handling food

When traveling in areas where food is likely to be contaminated, wash, peel, or cook all raw vegetables and fruits w/safe water before eating

Microsporum canis, Microsporum gypseum

Trichophyton mentagrophytes, T. verrucosum, T. equinum

Epidermophyton (Tinea: humans only)

A few are soil inhabitants (geophilic) e.g Microsporum gypseum, and cause disease in animals that are exposed while digging or rooting.

Other species are host-adapted to humans (anthropophilic) e.g. Tinea rubrum and Epidermophyton, and infect other animals rarely

The most important animal pathogens (zoophilic) worldwide are M. canis, M. gypseum, T. mentagrophytes, T. equinum, T. verrucosum and M. nanum

M. canis, M. gypseum, T. mentagrophytes, T. equinum, t. verrucosum, M. nanum

M. canis infections of domestic cats and T. verrucosum of cattle and lambs especially

Cat - Microsporum canis (majority of zoonotic ringworm infections caused by this and contracted from cats)

Dog - M. canis

Horse - T. equinum & T. mentagrophytes

Cattle - T. verrucosum

Swine - M. nanum

Sheep - T. verrucosum

Rabbits, rodents - T. mentagrophytes

The fungal species

Host factors - such as age, immunocompetence, condition of exposed skin surfaces, host grooming behavior, nutritional status

Only in keratinized tissue and advancing infection stops on reaching living cells or inflamed tissue.

As inflammation and host immunity develop, further spread of infection is inhibited, although this process may take several weeks

Healthy adults - dermatophytes infections are self-limiting

Young/Debilitated animals - infection may be persistent and widespread (also see this in long-haired breeds of domestic cats)

May have a classic "ringworm" appearance

May mimic many other skin diseases

1. Fungal culture:  most accurate - Dermatophyte test medium (DTM)

2. Wood's lamp:  screening examination for M. canis infections in cats and dogs.  Only 80% of M. canis infections fluoresce.  False-positive examinations may occur

3. Direct microscopic examination of hair or skin scale

ALWAYS ask the client if anyone else in the household has pruritus or lesions similar to those on the pet.  Do NOT diagnose or suggest treatment for anyone other than the patient.

Not all ringworm in humans in zoonotic!!

In the great majority of cases the fungus gains entrance into the body thru trauma to the skin w/some kind of plant materials such as thorns or splinters.

Zoonotic transmission is also possible

The first symptom is usually a small painless bump resembling an insect bite.  It can be red, pink, or purple in color.

The bump (nodule) usually appears on the finger, hand, or arm where the fungus first enters thru a break on the skin.

This is followed by one or more additional bumps or nodules which open and may resemble boils.

Eventually lesions look like open sores (ulcerations) and are very slow to heal.

Limited to the skin.

Cases of joint, lung, and CNS infection have occurred but are very rare.  Usually they occur only in persons w/previous disorders of the immune system

Transmissible spongioform encephalopathies (TSE)

Rare brain diseases affecting mammals

Causes vacuoles in brain tissue (spongioform encephalitis)

Infectious agent is a protein (no RNA or DNA)

Prions are normal cellular proteins that misfold, resulting in aggregates that damage brain tissue

Prions replicate by acting as "pathological chaperones"

Scrapie - sheep

TME (transmissible mink encephalopathy) - mink

CWD (chronic wasting disease) - deer, elk

BSE (bovine spongiform encephalopathy) - cattle

CJD - Creutzfeld-Jakob Disease

vCJD - variant CJ disease (caused by BSE)

FFI - Fatal familial Insomnia

Kuru

Alpers Syndrome

GSS - Gerstmann-Straussler-Scheinker syndrome

PrP = "Proteinacous Particle" - the name given to this infectious protein

PrP^C - normal cellular form of the protein

PrP^Sc - form protein found in Scrapie diseased sheep

Cell surface glycoprotein involved in signaling or adhesion

PrP contains a high affinity binding site for copper ions - may be involved in copper transport/metabolism; conserved in many species (from humans to yeast)

When an abnormal prion protein is introduced into neural tissue, it interacts w/normal "cellular" prion proteins and causes them to misfold into the abnormal conformation.  Thus a single misfolded protein can result in the appearance of millions of copies of the abnormal protein.

The abnormal protein is less soluble and more resistant to enzymatic degredation than the normal protein

1. Through horizontal transmission from e.g. a sheep to a cow (BSE)

2. In inherited forms, mutations in the prion gene are transmitted from parent to child

3. The can arise spontaneously

Loss of motor control

Dementia

Paralysis

Wasting

Pneumonia

Death

Long Incubation Period

Extended Preclinical Period

Progressive Neurologic Dysfunction

Fatal

No Treatment

No Vaccine

High infectivitiy - brain, spinal cord, eye

Medium infectivity - lymph nodes, spleen, tonsils, placenta, CSF

Low infectivity - bone marrow, liver, lung, pancreas, nasal mucosa

No detectable infectivity - milk, saliva, bone, hair, skin, urine

Uncertain - blood, muscle

They secrete prions into the milk and infect nearly 90% of naive suckling lambs.

Thus, lentiviruses may enhance prion transmission, conceivably sustaining prion infections in flocks for generations.

The study also indicates a risk of prion spread to sheep and potentially other animals thru dietary exposure to pooled sheep milk or milk products.

Autoclaving - reduces, does not eliminate

Boiling - reduces, does not eliminate

Phenol - effective

NaOH - effective

50% Bleach - effective

1. Assay must distinguish abnormal (PrP^Sc) from normal (PrP^c)

Difficult b/c have identical AA sequence just different tertiary structure

2. Protease sensitivity

PrP^C sensitive to proteinase K digestion

PrP^Sc resistant to proteinase K digestion

3. Immunohistochemistry (IHC)

Need obex (brain stem), lymph, or tonsil tissue ~ 10 microns thick sections

Antibody reaction - prion protein antibody; ovine

Fixed tissue - formalin (10%) fixation; 1-3 day fixation

2nd antibody labelled w/horseradish peroxidase

Positive reaction - infected animal

Negative reaction - abnormal protein not detected; animal may be infected

Occurred many years after eating dead relatives

Lack of coordination

Slurred speech

Coma

Death w/in 6-12 months of first symptoms

Much more common in women then men

Proved that Kuru was not a genetic disease by taking brain material from Kuru infected brains of dead Fore and injecting this into the brains of monkeys who developed Kuru like symptoms.

Initially called it a slow virus disease due to the long incubation period.

Convinced the Fore to give up cannibalism, and now Kuru is extinct

Bovine Spongiform Encephalopathy (BSE)

A progressive neurological disorder of cattle that results form infection by a prion

Possibly originated as a result of feeding of scrapie-containing sheep meat-and-bone meal to cattle

There is strong evidence and general agreement that the outbreak was amplified and spread thruout the UK cattle industry by feeding rendered bovine meat-and-bone meal to young calves

December 2003

Cow was imported from Canada in August 2001

A UK program that excludes all animals more than 30 months of age from the human food and animal feed supplies.

The program appears to be highly effective

Negligible BSE risk

Controlled BSE risk

Undetermined BSE risk

Risk assessment

Surveillance

1 of 3:  No BSE cases; only imported cases; indigenous BSE cases born no more recently than 11 years

Existing education and reporting program

Feed ban in place for at least 8 years if a case or risk factors exist

Countries w/indigenous BSE cases must demonstrate an education and reporting program and an effective feed ban

Both negligible risk and controlled risk countries must also identify, track and prevent birth cohort and feed cohort of the known BSE-infected animal(s) from entering the food and export trade

Live cattle selected for export are identified by a permanent identification system and the cattle selected for export are born after a feed ban was implemented

A controlled risk country in regard to BSE

Means that US regulatory controls are effective and that US fresh beef and beef products from cattle of all ages can be safely traded