LECTURE 14: Emerging and Zoonotic Diseases

endemic diseases

tuberculosis

respiratory infections

diarreal diseases

malaria

helminths (worms)

emerging/reemerging diseases

aids

mutidrug resistant TB

dengue

hanta (HPS)

lyme disease

ebola

leptospirosis

cholera in the americas

covid 19

key factors in endemic diseases

poverty

poor sanitation/hygiene

malnutrition

overcrowding

key factors in emerging diseases

international trade and travel

economic development and land use

• deforestation

• new roads, mines, plantations

• contact with wild animals

ecological and climate change

behavioural and demographic cange

technology and industry

microbial adaptation (antibiotic resistance)

breakdown of public health

susceptibility: lack of immunity

the convergence model

factors influencing the outcome of microbial infections

center of the box represents the convergence of factors leading to the emergence of infectious disease

black center represents unknown factors: “black box”

model indicates that all factors are interlocking

zoonotic infection

a human infectious disease originating from an animal reservoir and not requring the human as part of its life cycle

• infectious agent/disease that can successfully circulate among animals without the host

• diseases where human is required for life cycle are NOT zoonotic

  • helminths

  • other infections with animal intermediate

current zoonotic diseases may be due to…

more recent exposure of humans to microorganism

slower evolution of host-parasite relationship

Diseases that were zoonootic, but now exclusively human

small pox virus evolved from camelpox virus

measles virus from reinderpest virus of cattle

mycobacterium tuberculosis from M.bovis

HIV from SIV (simian immunodeficiency virus)

ebola virus

linear non-segmented ss - RNA genome

filovrius: appears as filamentous particles in the shape of a hook

first discovered near ebola river in Congo

ebola virus: natural reservoir

fruit bats in the Pteropodidae family are considered the natural host

ebola virus: transmission TO humans

transmitted to people from wild animals

close contact with blood, secretions, organs, or other bodily fluids of infected animals

in africa, infection has been documented through the handling of infected champanzees, gorillas, fruit bats, monkeys, forest antelope, and porcupines found ill/dead in rainforest

ebola virus: transmission AMONG humans

direct contact with blood or bodily fluids of an infected symptomatic person

exposure to objects (needles) that have been contaminated with infected secretions

viruses often spread through families and friends that come in close contact with infectious secretions when caring for ill persons

ebola virus: transmission in health care settings

hospital staff not wearing appropriate protective equipment: masks, gowns, gloves

lack of proper cleaning and disposal of instruments (needles, syringes)

• inadequate sterilization of instruments reused

symptoms of ebola

treatment of ebola

balance pateints fluids and electrolytes

maintaining oxygen status and blood pressure

treating for any complicating infections

monoclonal antibodies

ebola prevention

express ebola glycoprotein on surface of vesicular stomatitis virus (VSV), a benign virus that causes asymptomatic or mild flu-like symptoms in humans

rabies

ss - RNA, enveloped virus

rhabdovirus: rod/bullet shaped

most deadly infectious disease known

does not follow iceberg pattern

reservoirs of rabies

wild and domestic animals

• rabid cat

• fox

• bat

• mongoose

• racoon

• skunk

transmission of rabies

virus shed into saliva and transmitted when animal bites the human

enters via animal bite/skin break, replicates locally, migrates to neurones

may also be transmitted via exposure to bat feces

pathogenesis of rabies

virus multiples initially in tissue around bite

travels up nearby peripheral nerves to brain (1-3 months), then destroys cells in the CNS

moves to salivary glands

clinical manifestations of rabies

spinal cord, brain: acute encephalitis

infection to symptoms: 20-60 days

pain at site of wound: bat bites may be painless

neck pain around 2 months later

loss of control of movement

throat muscle paralysis: difficulty swallowing

• drooling

• hydrophobia (fear of water)

behaviour change: extreme agitation

coma

death 3 months after exposure

diagnosis of rabies

usually after death, using autopsy material from animal or human

• negri bodies in the brain

• PCR of brain / other material

samples taken from wound

• fluorescent antibody test

• PCR

treatment of rabies

no established antiviral treatment available

immunological treatment:

• passive immunization injected

• active immunization with inactivated vaccine; 2 injections in the arm, each 1 week apart

  • secondary prevention

  • virtually 100% effective

rabies prevention

animal control

• required vaccinations of dogs

• quarantine of imported animals in countries/areas that are rabies free

• wildlife surveillance and reducing stray, unvaccinated dog and cat population

vaccination of people at risk of exposure

• occupational

  • outdoor work with wildlife exposure

  • laboratory personnel

• travelers to high risk areas

education of the public

toxoplasmosis

Toxoplasma gondii

protozoan parasite

Apicomplexa phylum

reservoir: cats and other feline

definitive host: cat

reservoir of toxoplasmosis

cats and other felines

transmission of toxoplasmosis

cats are definitive host: sexual cycle occurs only in intestine of feline family

transmission occurs from ingestion of material contaminated with cat feces

bird, rodents, ungulates, humans are intermediate hosts

• T.Gondii forms cysts in their tissues

• transmission can occur from eating undercooked beef

toxoplasmosis epidemiology

ubiquitous

• invades all cell types

• worldwide zoonosis

seropositivity increases with age

opportunistic infection associated with AIDS

clinical manifestations of toxoplasmosis

infection in most adults asymptomatic due to control by the immune system

infection severe and possibly fatal in immunocompromised individuals due to encephalitis, neurologic diseases

small children: fever, rash, pneumonia, encephalitis

toxoplasmosis effect on fetus

T.gondii can cross placenta in 40% of fetuses of non-immune mothers

• mismarriage

• 12% of babies die shortly after birth

• <20% are normal after age 4

• damage to central nervous system

  • hydrocephaly

  • blindness

  • mental impairment

  • motor disturbances

diagnosis of toxoplasmosis

direct smear of material from spinal fluid or blood

ELISA serum antibody test

PCR

treatment of toxoplasmosis

sulfonamides, pyrimethamine, sulfadiazine (inhibit folic acid synthesis)

protozoans need folic acid in greater quantity than host cells

prevention of toxoplasmosis

avoid eating raw or undercooked meat

prophylactic antimicrobials for a non-immune pregnant woman who has been exposed

don’t have a cat, or have an indoor-only cat

if there is an indoor-outdoor cat

• use hygienic food preparation practices

  • keep cats off kitchen counters and eating table

  • wash hands between handling cat and preparing food

• be cautious in handling kitty litter

  • pregnant women should not empty kitty litter

effect of toxoplasmosis on mice

mice infected with toxoplasmosis lose their instinctive fear of the smell of cats

parasites effect may be permanent

toxoplasma and behaviour manipulation in animals

animals: greater predation of intermediate host by definitive host

• increased non specific movements, more active

• reduced neophobic behaviour (less fear of new scents, sounds)

• reduced aversion (fatal attraction) to cat urine

• reduced learning behaviours

toxoplasma and behaviour manipulation in humans

humans (chronic infection)

• schizophrenia

• suicide attempts associated with seropositivity to T Gondii

• epilepsy

• Congenital toxoplasmosis may reduce brain function

• loss of psychomotor performance

• men become more jealous, emotionally unstable, suspicious, short tempered, low self esteem

• women and men more anxious

plague

Yersinia pestis

gram - cocobaccilius

reservoirs: praire, rat, chipmunk, squirrel

transmission of plague

requires the flea as a vector

• bacteria multiply in flea gut and block it, causing flea to regurgitate infected material when flea feeds on a new host

• flea is in a starving state so bites frantically

bubonic plague

• Y. pestis multiplies in lymph fluid and lodges in lymph node nearest the site of flea bite

• bubo = enlarged lymph node black from hemorrhage and fever occur within 2-6 days

• disease not communicable among humans at this stage

pneumonic plague

occurs in 5% of plague cases

bacteria enter blood and disseminate to lungs, causing pneumonia

within 1-3 days skin becomes bluish to black from hemorrhage and lack of oxygen (black death)

disease is communicable among humans in this stage through respiratory route

mortality virtually 100% within a few days if early treatment not given

diagnosis of plague

patient sample from a bubo or gram stain (gram - coccobacillus)

direct smear made with laboratory antibody bacteria

rapid dipstick test for field testing of humans measures Y.pestis in human blood reacted with laboratory antibody to Y.pestis

treatment of plague

lancing/drainage of buboes

steptomycin, doxycycline, other antimicrobials

treatment effective if given early enough but diseased may not be recognized early enough

prevention of plague

surveillance for dead rodents in endemic areas

• if surveillance shows positive animals, rodent extermination in residential areas

posting of warning signs

inspection of ships for rats to prevent transport to a new area

rat guards on mooring ropes

education of tourists not to feed squirrels and chipmunks out of their hands

use insect repellant outdoors in endemic areas

prophylatic antimicrobial after probable exposure

vaccination for people in high risk occupation

anthrax

bacillus anthracis

large, gram + bacilli, facultative anaerobe, endospore forming

• endospores only form under aerobic conditions

zoonotic disease

herbivores: sheep, goats, cattle, reindeer - acquired for contaminated soil

carnivores infected from consuming meat

reservoir: animals (contaminated soil)

transmission of anthrax

human: contact with endospores during occupational exposure on farms/industries= wool, hides, meat, bones

wool sorters disease: respiratory anthrax

clinical manifestations of anthrax

cutanous anthrax: skin lesions, center black and necrotic

intestinal anthrax: symptoms mimic food poisoning

• lesions/ulcerations in digestive tract

• can lead to septicemia and death

• outbreak from unpasteurized goats milk cheese

respiratory: most deadly; most concern with bioterrorism

• symptoms similar to flu

• inhaled into lungs, spores germinate in alveoli

• phagocytized by macrophages, replicate

anthrax diagnosis

blood culture

gram stain

culture of external lesions

serological tests

PCR assays

treatment of anthrax

ciprofloxacin (fluoroquinolone)

penicillin

doxycycline

erythromycin

prevention of anthrax

human vaccine: 6 doses over 18 months

reduce exposure to endospocres

dispose of infected animals properly

vaccinate animals

one health triad

encompassing the collaborative goals providing optimal health for people, animals (domestic and wild) and the environment by considering interactions between all 3 systems