Zoonotic Diseases

Lecture 5Dr. Paul Bartlett, MPH., DVM., Ph.D.

Hantavirus Pulmonary Syndrome (HPS)

The first recognized cases occurred in May of 1993, in the four corners area of the southwest USA.– New Mexico, Arizona, Colorado, Utah

Through June 6, 2002 there have been a total of 318 cases of HPS in the USA.

38% of all reported cases have resulted in death

Cases have been reported in 31 states, including most of the western ½ of the country, and some eastern states– Over half of the cases of HPS are found outside the

four corners area.

Hantavirus Pulmonary Syndrome

Cases of HPS have also been confirmed from Argentina, Bolivia, Brazil, Canada, Chile, Panama, Paraguay, and Uruguay.– HPS is classified as a

pan-American zoonosis

HPS has also been linked with hypertensive renal disease in the inner city

Carriers in the USA and the virus they transmit:

Deer Mouse Sin Nombre virus - most often

Cotton rat (Florida) Black canal virus

Rice rat (Louisiana) Bayou virus

White footed mouse (New York) SNV

Bat viruses in Australia All of the newly identified viruses are

Rhabdoviruses which are related to the viruses that cause rabies and Lyssa fever.– Viruses in this family have a high fatality rate

often near 100% Henda Virus (Equine Morbillivirus) - infects

humans, horses, cats and Guinea pigs. Fruit bats are the natural reservoir.– Fast response to outbreak in Australia

Australian bat lyssa viruses (Ballina virus) - this is a close relative of rabies

Menangle virus - carried by fruit bats and causes disease in pigs

Dog and Cat Roundworms

(See assigned reading)

http://www.dpd.cdc.gov/dpdx/HTML/Toxocariasis.htm

(All 6 parts – “Causal agent” through “Treatment”)

Raccoon Roundworms (Baylisascaris procyonis)

Common intestinal roundworm of raccoons Eggs deposited in raccoon feces (infective in

thirty days) Ingested by man or other animal Aggressive migration (eyes, brain, other

tissue)– Fatal nervous system disease, eye

disease in intermediate host (mice, squirrel, chickens, quail, man etc.)

– Encyst and await ingestion by raccoon scavenger.

Raccoon Roundworms (Baylisascaris procyonis)

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5051a1.htm

(Skim the two cases, but read the “Editorial Note”)

Raccoon RoundwormsTransmission of Baylisascaris to

Humans

Eggs shed in raccoon feces, infective in 30 days

Hatch after ingestion, penetrate intestinal wall

Migrate to liver, lungs and muscle Encyst in small fibrous nodules

causing no further problems or Some enter the brain and eyes and

cause disease.

Raccoon RoundwormsPrevalence of Baylisascaris in

Raccoons

50- 89% of raccoons have the worm One study of 520 raccoons 70% of all age

groups and 88% of juvenile raccoons were infected.

Eggs are very resistant and can survive three to five years.

Serious infection is rarely diagnosed; <30 cases reported. Probably many undiagnosed cases.

Raccoon RoundwormHuman infection

Ocular infection– Primate research – multifocal retinal hemorrhages,

white spots, chorioretinitis, inflammatory tracks, vascular sheathing, and diffuse retinal degeneration

– Reaches eyes by 7 days post-ingestion Diagnosis of Baylisascaris infection

– History of pica, raccoon exposure

– Serology (still experimental- ELISA & Indirect immunofluroescent test).

– Difficult to diagnose in a living person but in ocular cases there is often a diagnostic lesion in the eye.

Raccoon RoundwormsControl and/or Prevention of

Baylisascaris

Disinfectants for contaminated areas (heat or lipid solvents)

Discourage raccoon ownership (pets)

Regularly de-worm raccoons at zoos, wildlife exhibits, etc.

Discourage raccoons from living near people by removing sources of food and/or shelter

Other Similar Roundworm Species

Skunk roundworm (Baylisascaris columnaris)– Poorly understood – Kills mice, rabbits, and woodchucks

by CNS migration– Infection of man is unknown

Viral Hemorrhagic Fever Caused by a number of viruses – Lassa,

Marburg, Ebola, and Congo-Crimean Hemorrhagic Fever

Most are transmitted by direct contact of bodily fluids in the later stages of the disease – Vomiting, diarrhea, shock and hemorrhage.– not transmissible via air.– Caregivers often infected.

Ebola and Marburg are RNA viruses in the filovirus family.

Electron micrograph of

Ebola virus. 

biosafety level four (BSL-4) pathogens

Marburg First occurred in Germany in 1967

when Laboratory workers were exposed to infected monkeys from Uganda.

Non-human primates can be infected but they are not considered to be the natural reservoir.– The natural reservoirs for this virus is

unknown.

Ebola First discovered in 1976 near the Ebola river. There are four known types of the Ebola:

Zaire, Sudan, Ivory Coast, and Reston The Zaire and Sudan strains are associated

with disease in humans.– Incubation period is up to 3 weeks. – Initial clinical signs include fever, headache,

chills, myalgia, and malaise. Later abdominal pain, vomiting, diarrhea and occasionally a maculopapular rash are seen. Hemorrhagic manifestations with disseminated intravascular coagulation can be observed in fatal cases.

Zaire and Sudan strains (Continued)

– 50- 90% fatality has been reported.– Since its discovery in 1976, Ebola

has killed more than 800 people.– Due to the high fatality of the

disease, the outbreaks have not become large.

Zaire and Sudan strains (Continued)

Like Marburg, the natural reservoir is unknown but human cases are often preceded by large die-offs of non-human primates. Epidemiologists, including veterinarians, are currently investigating many sources including plants as possible vectors.

The last known cases of Ebola occurred in The Republic of the Congo and Gabon in late 2001 to 2002. – As of 4/1/2002, these outbreaks took the lives of 96

people in 122 known cases (WHO).

Personal Safety Issues

Veterinarians chasing around the jungle for Ebola

EIS Track record “Outbreak” the movie

Ebola - Reston (“The Hot Zone”) This strain of Ebola was discovered in Reston,

Virginia in 1989. It was first identified in monkeys from the

Philippines. Ebola-Reston is often fatal in monkeys, in four

known cases in humans however the virus evokes an immune response but was asymptomatic.

Four episodes of Ebola-Reston infection among monkeys imported from the Philippines have occurred in the USA and Italy.

Aerosol spread, while not documented in humans, has been seen in non-human primates. – Very scary!

Brucellosis Undulant Fever, Mediterranean Fever, or Malta Fever. Species of Brucella and the usual host.

– B. canis in dogs– B. melitensis in goats and sheep– B. suis in pigs– B. abortus in cattle

B. melitensis is the most virulent in humans and infection

is usually associated with unpasturized dairy products from Mediterranean countries or Mexico Incidence of human infections:

1947 - 6300 cases a year1990 – about 100 cases a year (but only 4 to 10% are recognized and reported).

Brucellosis Human cases:

– Incubation period- usually 30 days but can be up to 5 months

– Symptoms - non-specific. Fever, chills, headache, myalgia, arthralgia, anorexia, fatigue, lymphadenopathy and splenomagaly. The ratio to subclinical to clinical cases is 1:1 to 12:1.

– Treatment - many different antibiotics - Doxycycline Occupational exposures are common. Occupational exposure is seen among packing plant workers, veterinarians, livestock producers, and laboratory workers. Vets used to get strain 19 (vaccine)

– Exposures occur through breaks in the skin, inhalation and conjunctival contact.

Brucellosis Prevention:

– Reduce exposure by controlling the disease in the animal population.

– Public health efforts to ensure the proper pasteurization of dairy products.

Eradication Programs:– Cattle Brucellosis program - the goal is

eradication. Most of the infected herds are in Texas and the South Eastern states.

– Swine Brucellosis program – Nearly eradicated from US.

Bartonellosis

Two diseases: Cat Scratch Disease and Bacillary Angiomatosis.

Cat Scratch Disease has been described for 100 years. The agent, slightly curved gram negative rods, was identified in 1988.

The agent has been placed in the genus Bartonella – may be related to the agents which cause

Typhus, RMSF, tsutsugamushi, Q fever, Brucella, and Richettsia quintana.

CSD The disease is subclinical in cats. Transmission to humans:

– Following cat bites, scratches, and possibly bites

from cat fleas.– Cat saliva over an area of compromised skin

integrity may also lead to infection.– Kittens are more likely to infect people because

they scratch more often and have a higher prevalence of Bartonella.

– Prevalence in cats of all ages can be 30 to 50%.

CSD

An estimated 22,000 cases occur in the USA each year.

First a 2-3 mm macule occurs at the site of exposure. The macule becomes papular within a few days.

The duration of the disease is usually several weeks

Regional lymphadenopathy may develop with fever, fatigue, and headache.

Clinically it can look similar to tularemia or bubonic plague.

CSD

14% of cases can progress to more severe symptoms which can include eye problems, encephalopathy, arthritis, osteolysis, vascular system lesions, hepatitis, or pneumonia.

Treatment:– Uncomplicated cases resolve on their own.

– Antibiotics are effective in more severe cases.

Bacillary Angiomatosis Mostly in HIV - infected and other immuno-

suppressed individuals. Much more severe disease than is CSD.

– Vascular lesions may involve many organs, with skin being the most common.

Prevention:– Wash hands after handling cats.– Do not encourage rough play with cats.– Use flea control.– Do not let cats lick areas of abraded skin or open

wounds.– HIV patients may wish to avoid being scratched by cats.

Are CSD and Bacillary Angiomatosis caused by the same agent?

Despite the similarities in histochemical staining properties and epidemiology, serious reservations remained concerning a possible link between the causative agents of CSD and BA.

The pathologic features of classical CSD (granuloma) and BA (proliferative vascular lesions without granuloma) are distinctly different.

The two diseases seem to respond differently to antibiotic therapy. – The majority of BA patients evaluated responded quickly to single-

agent therapy with either erythromycin or doxycycline (14,23), whereas the symptoms and signs of patients with CSD failed to show consistent rapid resolution following antibiotic therapy.

Rat Bite Fever The responsible agent is Streptobaccilus

moniliformis (more common in U.S.) or spirillary RBF by Spirillum minus

Nasopharyngeal carriage rates in healthy laboratory rats range from 10% to 100%; carriage rates in wild rats range from 50% to 100%

Transmission is usually through a rat bite. However, some cases have rat exposure but no reported bite.– Ingestion of food contaminated with rat feces

Children and laboratory workers are at high risk to contract this disease.

Cases are rarely reported in the United States and the true incidence of disease is unknown.

Rat Bite Fever

Clinical syndrome: 2-10 days after rat bite.

Usually a mild protracted illness with a fever, malaise, cough, maculopapular rash, and occasionally arthritis.– Human fatalities have been reported.– Antibiotics are effective (Shot gun)

Susceptible to penicillin diagnosed by blood culture only.

Lymphocytic Choriomeningitis Virus (LCMV) The main reservoir is the house mouse (Mus musculus)

but hamsters and domestic mice can also be infected. Infection in people:

– Often subclinical.– “influenza-like symptoms” but sometimes

meningeal symptoms of a stiff neck, fever, headache, malaise, and muscular pain.

– Incubation period - 1 to 2 weeks. – Pregnant women may transmit the disease to the

unborn fetus resulting in fetal or neonatal death, hydrocephalus, chorioretinitis, or psychomotor retardation.

Usually a history of a febrile illness during their pregnancy.

LCMV Prevalence- a study in Baltimore showed

that 9% of house mice and 4.7% of residents had LCMV antibody

Transmission:– Contact with mouse nasal secretions, urine,

semen, milk, and feces– Mouse and hamster bites.– Humans become infected by inhaling

infectious aerosolized particles of rodent urine, feces, or saliva, by ingesting food contaminated with virus, by contamination of mucus membranes with infected body fluids, or by directly exposing cuts or other open wounds to virus-infected blood.

LCM Risk factors:

– Recreational activates in rural environments.

– Habitation in older rodent-infected homes.

– Acquisition of rodents for pets– Laboratory exposure to unscreened

rodents (rare)– Pregnant women risk exposure to their

unborn children.

LCMV Epidemiology of LCMV in mice:

– Much studied, interesting epidemiology, when LCMV is introduced to a non-infected colony.

– Adult mouse infection shows some morbidity, but most recover and no longer shed the virus.

– Infections acquired in utero lead to a persistent tolerant infection with heavy shedding throughout their lives (similar to BVD in cattle).

– Over time, the infection was only transmitted congenitally in that all mice had been infected before they were born.

– It appeared that transovarian infection was the rule, rather than the exception.

LCMV

Prevention:– Control the mouse population in

houses.– Don’t touch dead mice.– Pregnant women should avoid

hamsters, and other rodents.– Most all laboratory animal colonies in

the US are LCMV-free.