Zoonoses Norris 5/30/15

( * = Alternative Portals Possible) Zoonotic Infections

Modes of Transmission Bacterial Viral Parasitic Fungal / Other
Orf, Vesicular stomatitis, Nematoda (GI), Strongyloides
Anthrax*, Brucellosis*, Erysipeloid,
Direct Contact Hemorrhagic fevers (MERS-CoV*, (UGI, AIDS), Schistosomes, Dermatophytes
Leptospirosis, Glanders*, Tularemia *
Ebola*) Trematodes
Animal Bites and Scratches Pasteurellosis*, Cat scratch fever Rabies Blastomycosis
Anthrax*, Ornithosis, Plague*, Q Fever, Lymphocytic Choriomeningitis,
Inhalation Histoplasmosis
Tuberculosis*, Tularemia* Hantavirus pulmonary syndrome
Brucellosis*, Campylobacter (GI),
Trichinella (SBM), Toxoplasma, Variant Crutzfeldt-Jakob disease
Ingestion Listeriosis*, Salmonellosis (GI), Norovirus, (Ebola & Marberg HF?)
and other food-borne trematodes (vCJD)
Tuberculosis* (RTI), Yersiniosis
Fecal-Oral Salmonellosis (GI), Leptospirosis Norovirus (GI), Hepatitis A &E Toxoplasma, Toxocara
Lyme disease, Plague*, Relapsing fever, Yellow fever, Viral Encephalitis,
Arthropod Bites Tularemia*, RMSF, Scrub Typhus, Crimean-Congo, Yellow Fever, Babesiosis, Leishmaniasis (SMB)
Rickettsial Pox, Ehrlichiosis Dengue Hemorrhagic Fever

Regarding Species Listed Above But Not Expanded Upon Below… Anthrax —> Bacillus Anthraces

Only Including Information Covered in Zoonosis Lectures (Assume Covered Elsewhere)!
Brucella Species
• Gram (-ve), non-motile short rods.
Overview • Nutritionally fastidious: Facultative intracellular parasites; require complex artificial
media in-vitro; slow-growing (up to 10 days on blood agar).
• B. melitensis — Goats, sheep, camels (Europe, Asia, Middle East, S. and C. America).
• B. abortus — Cattle (Africa, Asia, South America).
Species
• B. suis — Pigs (South Asia)
• B. canis — Dogs
• Reservoir—>Animal excretions (milk, urine, feces, vaginal discharge, uterine products).
Epidemiology • Transmission —> Direct occupational exposure (butcher, vets) or ingestion of
contaminated dairy products (killed by pasteurization).
• Skin penetration/ingestion —> phagocytosis (inhibit lysosome-phagosome fusion in
PMN) —> localize to reticuloendothelial system —> Failure of T cell response leads to
granulomatous inflammation with bacterial multiplication —> waves of bacteria released
from site (recurrent bacteremia).
• Acute: Incubation (7-21 days) —> Undulant fever (onset with drenching sweat and high
fever, then a swinging fever, rigors, lethargy, headache, musculoskeletal pain, scrotal
Pathogenesis
pain) —> Occasionally delirium, abdominal pain, constipation —> Lymphadenopathy and
splenomegaly.
• B. melitensis: most severe; B. suis: abscess formation.
• Infection is localized in 30% cases (especially w/ delayed diagnosis & treatment).
• Chronic: Episodes of nocturnal fever persist for months or years —> marked weight loss
— Osteomyelitis = most common complication —> sacro-ileitis —> depression.
• Isolation blood cultures; (+ve) 75% of cases with B. melitensis; 50% with B. abortus.
• Bone marrow may be useful in more chronic states.
Diagnosis
• CSF in neuro-infection: 30% culture positive.
• Risk to laboratory staff from culture; serology (Brucellergin skin test — DTH response)
• Large; box-car appearance; Gram (+ve) rod; aerobic; spore forming; non-motile serology.
• Only medically important bacteria with protein capsule (not polysaccharide).
Overview
• Native to hoofed domestic herbivores (cattle, horses, goats, etc.)
• Sought by various nations/groups as a biological weapon.
• Three proteins produced by genes carried by a large plasmid pXO1, which are non-toxic
individually but when combined become toxic.
• Protective Antigen (PA) —> binds cell membrane and mediates endocytic entry of EF or
LF (both inhibit host innate immunity)
Virulence • Lethal factor (LF) —> Stimulate macrophages to release TNF-α, IL-1ß, and other
Factors inflammatory cytokines.
• Edema Factor (EF) —> allows accumulation of fluid into tissue —> cell death.
• Polypeptide capsule (Poly-D-Glutamic acid).
• Three genes (CapA, CapB, CapC) on plasmid pXO2
• Only one serotype known — probably because of glutamic acid polymer.
• Spores enter human via:
• Cutaneous Abrasion —> Spores begin at site as a papule —> progress through a
vesicular stage to a depressed black necrotic ulcer (eschar).
• Ingestion —> Spores germinate/multiply in oropharynx or intestines —> dysentery.
Pathogenesis
• Inhalation —> Spores germinate and multiply in respiratory tract —> bacteremia —>
septicemia —> fever, dyspnea, non-productive cough —> near 100% mortality!
• Incubation period: 1-12 days.
• Fatality without antibiotic treatment ~ 20%; with treatment ~1%.
• Cutaneous (most common; least life-threatening)
• Septicemic (high mortality)
• Pulmonary (highest mortality in humans; “Wool-sorter disease”).
Presentation • Prodrome resembling “flu-like illness, characterized by myalgia, fatigue, fever, with or
without respiratory symptoms, followed by hypoxia and dyspnea (often with radiographic
evidence of mediastinal widening).
• Meningitis in 50% of patients; rhinorrhea is rare.
Dx & Rx • Culture of skin lesion or biopsy; Parenteral penicillin G.
 Zoonoses Norris 5/30/15

Erysipelothrix rhusiopathiae Phylum Platyhelminthes: Trematodes —> Shistosoma spp.

Species Schistosoma haematobium Schistosoma mansoni Schistosoma japonicum
Description • Diphtheroid-like rod; Sensitive to penicillin and erythromycin; Gram (+ve)
Biomphalaria Snails —
Bulinus Snails — Africa, Mid East, Oncomelania (Snail) — China,
Etiology Hosts S. America, Caribbean, Africa,
• Found in animals, meat, and seafood; Fishermen, butchers, veterinarians at risk. Indian Ocean Islands, India Philippines, Taiwan Indonesia
Madagascar, Mid East

Pathogenesis • Erysipeloid —> painful, slow spreading infection following traumatic inoculation. Presentation • Acute: Itchiness at site of penetration (see Swimmer’s itch — 0-3 days); fever, chills. lymphadenopathy.
• Chronic: Periportal fibrosis, intestinal polyps, bladder inflammation, hematuria, carcinoma.
Leptospirosis —> Leptospira interrogans Larva released by snails into fresh water —> Penetrate human flesh and enter bloodstream —> travel to
portal vein —> larvae mature into adults —> adult pairs migrate against portal flow into venous plexuses:
• Very common zoonosis; Ubiquitous in wildlife and domestic animals.
Overview • Spirochete; sensitive to heat, drying, and most chemicals. • In bladder venous plexus —> mate • In intestinal venous plexus —> mate —> release eggs —> acute
• Enters susceptible host by penetrating skin and/or mucus membranes. —> eggs released —> acute inflammatory response (Katayama fever, chills,
inflammatory response (Katayama lymphadenopathy) —> eggs exit into intestinal lumen —> passed
fever, chills, lymphadenopathy) —> into feces.
• L. ictero-haemorrhagia — rats. // • L. Canicola — dogs. Pathobiology
Other Species eggs exit to bladder & pass in urine. • Some eggs lodge in intestinal wall —> Chronic inflammatory
• L. hebdomadis — cattle. // • L. pomona — pigs. • Some eggs lodge in bladder wall — response —> intestinal inflammation and consequences (polyps)
> chronic response —> bladder • Note: Granulomatous colitis, bleeding, anemia; hepatic
• 1st phase (Leptospiremic phase): Host immune response —> flu-like symptoms, inflammation and consequences granuloma/fibrosis (Symmer’s Pipe-stem fibrosis), portal
photophobia —> resolves within a week as organism cleared. (hematuria, bladder carcinoma) hypertension, splenomegaly, hepatomegaly.
• 2nd phase (immune phase): Host immune response and rise in anti-leptospira IgM
Pathogenesis associated with mild or severe damage: Excreted eggs hatch in fresh water and infect snails.
• Anicteric leptospirosis (mild) —> aseptic meningitis.
• Direct: Eggs in urine. • History
• Weil’s disease (severe) —> vasculitis with hemorrhagic complications, kidney damage
• Indirect: Serology, gross hematuria • Direct — detection of eggs in stool or rectal biopsy
with renal failure, liver damage with jaundice. Diagnosis
w/ questionnaire microhematuria, • Indirect — Ultrasound liver, morbidity assessment. [S.j.- grading
morbidity imaging via ultrasound. of network fibrosis (liver calcification)]
• Four syndromes (after 1-2 week incubation):
• Bacteremia: Flu-like, diarrhea, and vomiting; conjunctival congestion. Praziquantel — treats bladder and kidney pathology
Clinical Treatment
• Meningitis: Aseptic meningitis. Control: VIP (Ventilated Improved Pit) latrines; For S.j — Immuninize water buffalo with Praziquantel
Presentation
• Icteric: Fever, hemorrhages, hepatic and renal impairment. • Younger age classes have the highest intensities of infection, highest exposure, exhibit least evidence of
• Pulmonary: ARDS resistance to infection.
Additional
• Schistosomal eggs highly immunoreactive; adult forms evade immune system by coating w/ host antigens.
• Spirochete in blood, CSF (1st phase), and urine (2nd phase). Facts
Diagnosis • Most bladder cancers are transitional cell carcinomas; S. haematobium-associated bladder cancers are
• Serology (PMN rise, liver enzyme rise, CK rise; platelet fall); CSF “viral pattern”; PCR. frequently stratified squamous carcinomas.

Tularemia —> Francisella tularensis Class Nemetoda —> See parasitology slides for more info.

• Gram (-ve) short rods; facultative; non-spore forming
• Nutritionally fastidious: will not grow on blood or other common media; requires
Overview supplemental compounds —> Cysteine-Glucose Blood Agar (aerobic).
• Slow growing —> requires 2-10 days for visible growth.
• Note: F. tularensis & BCG (TB) vaccines are only life-attenuated vaccines for bacteria.
• Small, wild mammals: rabbits, beavers, deer (can be found in cats/dogs).
Epidemiology • Ticks: Dog tick (D. variabilis), wood tick (A. americanum); Deer flies (Crysops spp.)
• A northern hemisphere disease (most cases occur Arkansas, Oklahoma, Missouri).
• Entry through inhalation, ingestion, or injection (minimum dose < 100 cells) —> bacteria
multiply locally —> papule forms —> develops into ulcer with black base (ulceroglandular
Pathogenesis
tularemia) —> bacteria phagocytosed —> localizes RES —> regional lymphadenopathy,
long-lasting fever.
• Incubation 2-5 days —> fever, chills, and malaise; Syndrome depends on site of infection:
Clinical • Ulcero-glandular (from injection: lowest mortality).
Presentation
• Typhoidal (resulting from ingestion: higher mortality).
• Pneumonia (from inhalation: highest mortality).
• Difficult because disease is rarely suspected; culture is difficult and risky to lab personnel.
Diagnosis Serodiagnosis: rise in agglutinating antibodies 1:40 to 1:320 in 1-2 weeks.
• Treatment — Aminoglycosides
• Multicellular, smooth spindle-shaped, tubular alimentary tract, distinct males and
Physiology
and Structure
females; Larvae are possibly aerobic while adults are anaerobic.
• Nutrition through ingestion or absorption of body fluids from the host.
Hookworms: • Fecal-cutaneous transmission —> infectious (filariform) larvae penetrate skin of
feet, causing local itching —> enter bloodstream; transported to lungs —> enter
Necator alveoli and ascend toward trachea —> respiratory tract inflammation (pneumonia
americanus
possible) —> larvae pass to pharynx & swallowed—> mature to adults in GIT —>
Ancylostoma
attach to mucosa via cutting plates or teeth —> may cause gastroenteritis
canium initially —> secrete anticoagulant and suck blood from host —> anemia.
• Cat/Dog hookworm can infect human; can’t invade bloodstream —> travel
A. braziliense subcutaneously = trail of itchiness until they die (cutaneous larva migrans).
• Pathogenesis: Blockage of internal organs; migration through tissues by larvae.
Ancylostoma • Immunopathogenesis: Protein losing entropathies; type I autoimmune disease.
• Avoids immune defense by concealment of antigenic sites.
• Most often asymptomatic; Respiratory: Dry cough and throat irritation;
Strongyloides
Abdominal: stomachache, bloating, heartburn; diarrhea & constipation; nausea;
Respiratory: Dry cough and throat irritation; Skin: An itchy, red rash that occurs
where the worm enters the skin.
 Zoonoses Norris 5/30/15

Pasteurellosis —> Pasteurella multocida Ornithosis —> Chlamydophilia psittachi

Overview • Gram (-ve), coccobacilli; facultative; fermentation (+ve); Oxidase (+ve); Catalase (+ve). Overview • Small, round, obligate intracellular bacteria, unique development cycle.

Epidemiology • Normal respiratory biota of many lower animals; humans are infected by bite or scratch.
• Sometimes also found in human sputum, so humans could transmit…
• Normally inhabits oral cavity of animals —> enters human skin via bite —> at inoculation
Pathogenesis site elicits inflammatory response —> spreads locally to soft tissue (cellulitis) and bone
(osteomyelitis) —> may progress to septicemia.
• Bipolar staining!
• Grows readily on enriched media like Blood Agar but not on media selective for Gram
Diagnosis
negatives (MacConkeys); confirm diagnosis by culture from aspirated pus.
• Sensitive to Penicillin
Cat Scratch Disease —> Bartonella henselae
Overview • Gram (-ve), coccobacilli, pleomorphic, silver impregnation stains.
• Facultative intracellular pathogens
Clinical • Regional lymphadenopathy, fever of unknown origin, ocular involvement,
Presentation hepatosplenomegaly, bacillary angiomatosis, organ-specific symptoms.
• Cats serve as natural reservoir —> inoculate humans via cat scratch, bite, or saliva —>
primary cutaneous lesion —> local infection causes regional lymphadenopathy.
• Disseminated infection (especially HIV/ immunocompromised) results in symptoms
depending on organ involved:
• Ocular: Parinaud’s oculoglandular syndrome, granulomatous conjunctivitis, periauricular
lymphadenopathy, optic neuritis.
Pathogenesis
• Skin: Bacillary angiomatosis (multiple subcutaneous enlarging red papules, resembling
cranberries; occur in viscera as well).
• CNS: Encephalitis, transverse myelitis, cerebellar ataxia.
• Musculoskeletal: Myalgias, arthralgia, arthritis, osteomyelitis.
• Liver/spleen: necrotizing granulomas causing hepatosplenomegaly, pelisses hepatitis
(blood-filled cavities throughout liver).
Diagnosis • Serology; blood cultures; PCR; biopsy showing granulomatous infection.
• Treat with Docycyline.
Related • Bartonella quintana, historically cause of “trench fever”, typically associated with bacillary
species angiomatosis, endocarditis, and fevers. Transmitted by lice; occurs in homeless patients.
Rabies Virus
Presentation • Dysphagia, encephalitis.
• Infects many mammalian species, including dogs —> transfers to human via animal bite —
> localizes to bite site for days to months —> binds to acetylcholine receptors and enters
peripheral nerves —> travels proximally to CNS (retrograde transport via dynein; distance
Pathogenesis
determines incubation time) —> infects neurons of brainstem and brain —> cytoplasmic
inclusions (Negri bodies) form —> cell necrosis —> cranial nerve palsies and encephalitis
—> dysphagia, agitation, seizures —> coma —> death.
• Skin biopsy: immunohistological staining — Rabies Ag // Neri bodies
Diagnosis
• Corneal smears: Rabies Ag; Direct antibody test —> Human Rabies Neutralizing Ab.
Treatment • Post exposure prophylaxis; wash wound immediately; HRIG Ab for passive immunity.
Blastomycosis
Virulence • No peptidoglycan in cell wall; instead LPS with weak endotoxicity.
• Major Outer Membrane Protein (MOMP) is major cell wall component unique to species.
Factors
• Outer Membrane Protein (OMP) is common to all chlamydia.
• Small infectious EBs attach to microvilli, follow by active penetration into cell —> remain
within cytoplasmic phagosomes —> Intact EB outer membrane inhibits fusion to the
Life Cycle lysosomes thus no killing of chlamydia —> 6-8 hours after penetration, EBs reorganize to
become large metabolically active RBs —> 18-24 hours later, the RBs divide to become
smaller EBs again, rupturing host cell.
• Spreads to the RES of liver and kidneys producing necrosis.
• Seeding in lung through blood causing lymphocytic inflammation in alveoli.
Pathogenesis
• Edema, thickening alveolar wall, inflammation of macrophages, necrosis, and hemorrhage.
• Mucus plugs the bronchioles causing cyanosis and anoxia.
• Transmitted to humans via inhalation of excreta, urine, or respiratory droplets of birds.
Epidemiology • Person-to-person transmission is rare.
• Vets, zookeepers, pet shop/poultry processing employees are at high risk.
• Incubation 5-14 days; headaches, high fever, myalgias.
• Pulmonary: non-productive cough and consolidation (atypical pneumonia).
Clinical
• CNS: encephalitis, convulsions, coma, and death.
Symptoms
• GI: nausea, vomiting, and diarrhea.
Other: Hepatosplenomegaly, follicular keratoconjunctivitis.
•
Prevention • Diagnosis is by serology; Iodine stain negative, Giemsa stain positive.
and Control • No vaccines available; treat infected birds/patients with antibiotics.
Yersiniosis —> Yersinia Pestis
• Gram (-ve) short bacilli; Gram (-ve); Oxidase (-ve); Facultative; glucose fermenter.
• Xenophylla cheopis (Rat flea) is main vector; virus dynamically maintained in rodents.
Overview
• Europeans with defective CCR5 sequence (1 gene mutation = resistance; 2 = immune to
HIV) —> lis back to survivors of Plague outbreak in Europe 700 years ago.
Virulence • Rich polysaccharide capsule present in virulent strains —> Safety-pin bipolar staining.
Factors • Capsular F-1 antigen: Prevents phagocytosis, generates Ab response.
• Transmitted from rodent to humans by flea vector —> phagocytosed —> transported to
regional lymph nodes —> multiplies and stimulates inflammation —> regional
lymphadenitis (buboes) often in groin.
Pathobiology • Within macrophages, capsular F1 antigen prevents phagocytosis —> intracellular
replication —> spread —> invades liver, spleen, skin, and lungs
• Endotoxin causes DIC —> cutaneous hemorrhagic necrosis = black color (black death).
• Pulmonary infection can be spread by respiratory droplets —> Pneumonic plague.
Prevention • Rat control; avoid handling, skinning wild animals in endemic areas.
• Post-exposure prophylaxis w/ cases of pneumonic infection is doxycycline 100mg or
and
ciprofloxacin 500mg bd for 1 week.
Containment
• Inactivated vaccine does not work against pneumonic plague.
• Incubation: Bubonic form is 4 to 7 days; Pneumonic form is 18-36 hours.
Clinical • Acute stage Bubonic Plague: Swollen, painful inguinal lymph nodes; increasing fever,
symptoms pooling of blood and micro hemorrhages in face and extremities.
• Acute stage Pneumonic: violent and fulminating bacterial pneumonia; nearly always fatal.

Mainly causes brain abscesses Diagnosis • Lymph node aspirate: An affected bubo should contain the organism; culture.
 Zoonoses Norris 5/30/15

Q Fever —> Coxiella burnetii Toxoplasmosis —> Toxoplasma gondii

• Used to be classified in family Rickettsiacea • Definitive host = felids (most important = domestic cat); 30% of the world’s population is
Hosts
• Obligate intracellular parasite; can survive in extracellular environment for a long time. infected.
Overview
• Phase variation: Phase 1: highly infectious w/ LPS; Phase 2: not infectious, truncated LPS
Morphology • Cresent-shaped trophozoites within macrophage.
• Incubation 3-4 weeks; most infections asymptomatic

• Carried in cattle, sheep, goats —> microorganism shed in animal products —> survives • Immunocompetent patients: Asymptomatic; Lymphadenopathy.
Pathobiology extracellularly as spore —> inhalation of spores —> mild atypical pneumonia —> may Presentation • Immunocompromised patients: Encephalitis; Chorioretinitis.
lead to hepatitis, chronic endocarditis (most common), osteomyelitis, encephalitis. • Congenital infection: Mental retardation; Chorioretinitis.

• Serological: Phase I and II — IgM break at 4-6 weeks. • Cysts ingested from undercooked meat or cat feces —> in small intestine, cysts release invasive
Diagnosis form —> penetrate wall —> phagocytosed and disseminated by macrophages —> infects,
• Weil-Felix negative
damages cells at distant sites —> host response contains infections —> in tissue, invasive forms
Treatment become dormant --> contained within cyst.
• Doxycycline (+/-) surgery for endocarditis. Pathobiology
• If host becomes immunocompromised —> cyst ruptures and releases invasive form --
>encephalitis, chorioretinitis, other infections.
Hantavirus (Sin Nombre) —> Bunyaviridae Hantavirus • If infection by pregnant mother —> invasive form crosses placenta to fetus —> congenital
toxoplasmosis —> mental retardation, chorioretinitis
• SS(-ve) RNA virus; enveloped; helical nucleocapsid.
Overview • Found in Far East, Scandinavia, E. Europe. • Indirect: Serology (IgM in infants, persons with first time, recent infection; IgG = life
• Severe pulmonary syndrome in SW USA. long immunity). Can also use CT, MRI of head.
Diagnosis
• Seroprevalence in adults increases with age, meat eating habits, # cats.
• Rodent hosts chronically shed virus in feces/urine —> airborne transmission to humans — • Direct: Tissue biopsy (trophozoites active, cysts dormant).
> viremia —> prodrome of flu-like symptoms followed by pulmonary capillary leakage —>
Pathobiology • TMP/SMX (Bactrim) + Pyrimethamine with Dapsone.
interstitial pulmonary edema —> respiratory failure (Hantavirus Respiratory Syndrome) —>
Treatment • Spiramycin prevents vertical transmission; prophylactic treatment of IgM+ pregnant mothers/
high mortality rate within ~10 days.
newborns.
• PCR from lung biopsy.
Diagnosis • Only pregnant mothers with an active primary infection can result in congenital toxoplasmosis;
• IgM antibody in serum. Additional Facts mothers with previous infections mount an immune response that protects the fetus.
• Pregnant mothers that are IgG (-ve) are encouraged to avoid cats.
Treatment • Supportive; no vaccines available.

Toxocariasis —> Toxocara canis Arthropod Bites

Hosts • Primary: Dogs // Intermediate: Humans Ixodes spp.: Lyme disease, Bebesiosis
•
• Ingesting soil with infection L2 eggs, liver and eye for humans, small intestine for • Amblyomma americanum (lone star tick): Causes African tick bite fever — Rickettsiosis
Transmission Tick Bites
puppies (definitive host) — PPP > 4 weeks. • Dermocentor spp. (Rickettsioses): RMSFQ fever Echricosis.
• Hyalomma sp. — Congo-Crimean H.F.
• Transmission to uninfected dogs can be by three methods:
1. Ingestion of feces/soil containing the L2 infective larvae. Mosquito Bites • Arboviral diseases: Yellow fever, dengue, chikungunya, and many others.
Life Cycle
2. Female dog prenatal infection through the placenta (vertical).
3. Transmammary infection (L3 larvae in milk).
Rickettsial Infections (Overview)
Diagnosis • Based on clinical symptoms and history
• Serological testing, ELISA, Ultrasound Disease Organism Vector Reservoir
• Visceral Larval migrans (VLM) — T. canis larvae migrate, without maturing, through
tissues. In liver, leads to hepatomegaly and eosinophilia. Rocky Mountain
R. rickettsii Tick Ticks, Rodents
• Affects primarily young children, lasts weeks/months. Spotted Fever
• Exhibits inflammation of internal organs and CNS.
Symptoms Epidemic Typhus R. prowazekii Louse, Fleas Humans, Flying Squirrel
• Patients can present with fever, cough, asthma, abdominal pain, nausea, fatigue, weight
loss, anorexia, headache, rash, and vomiting. Rarely, epilepsy, pleural effusion,
Scrub Typhus O. tsutsugamushi Mite Mites, Rodents
respiratory failure, and death have been reported.
• Ocular Larva Migrans (OLM) In the eye (blindness) — A granuloma forms around the
Ehrlichiosis E. Chaffeensis; E. ewingii Tick Deer
larvae in the retina, often resembling a retinoblastoma.

Treatment • Thiabendazole: Ultrasound for VLM and OLM; preventative antihelmintic for dogs Anaplasmosis A. phagocytophlium Tick Small Mammals

Control • Disposal of dog feces; restrict access to dogs in children’s areas. Q fever C. burnetii NONE (ticks in animals) Cattle, sheep, goats, cats
 Zoonoses
Rickettsial Species
• Most common tick-borne infections; intracellular Gram (-ve) organisms.
• Ask about activities that would place patients at risk of bites/contact with ticks,
Overview
lice, fleas.
• 3 main groups: Spotted fever, Typhus, and Scrub typhus.
• Primary infection in vascular epithelium (capillary leak syndrome), adrenal glands
affected
Common • Clinical manifestations: Sustained high fever, severe retro-orbital headache,
Features rash.
• Endotheliitis from endothelial cell infection leads to: Thrombosis and Eschar
formation.
• Rocky Mountain Spotted Fever: Bite of Dermacentor variabilis tick —>
organism infects and proliferates in endothelial cells (2-12 days) —> inflammation
of endothelial lining of small blood vessels, capillaries —> maculopapular rash/
R. rickettsii
petechiae on palms and soles spreading proximally to trunk (centripetal spread).
• Widespread necrotic vasculitis —> headache, encephalitis, renal & heart
failure.
• Mite-borne; Benign, self-limiting illness (2-3 weeks)
R. akari • Mites transmit from mice to humans —> papule at site of bite —> papule
vesiculates, fever, headache —> vesicle spreads over body (Rickettsialpox)
• Typhus Fever: Bite of Pedicures humanus louse that defecates when it feeds —
> organism infects and proliferates in endothelial cells (1-2 weeks) —>
inflammation of endothelial lining of small blood vessels, capillaries —> rash/
petechiae on trunk that spreads outward (centrifugal spread) but spares palms,
R. prowazekii soles, and face.
• Widespread necrotic vasculitis —> headache and CNS changes, gangrene —>
may lead to death if delayed treatment.
• If recover without antibiotics —> latent microorganisms may remain within cells
—> may cause recurrent, mild epidemic typhus (Brill-Zinsser disease).
R. • Chiggers (larvae of mites) transmit from rodent to humans —> scrub typhus
tsutsugamushi found in Asian and South Pacific; low mortality.
• Human Monocytic Ehrlichiosis: disease seems to be spread by Brown Dog Tick
in the US; often misdiagnosed as Rocky Mountain Spotted Fever.
E. canis & E. • Symptoms commonly include fever and GI abnormalities; Severe cases progress
chafeensis through cough, diarrhea, and lymphadenopathy up to respiratory insufficiency,
renal insufficiency, and CNS abnormalities; Detailed pathogenesis & pathology
unknown.
• Over 95%: fever, myalgia, headache; 75%: renal dysfunction; Less than 50%:
dyspnea, cough, confusion; Rarely: pancarditis, myocarditis, abdominal pain,
Anaplasmosis renal failure, ARDS.
• Lab findings: leukopenia, anemia, thrombocytopenia, trans-aminitis.
• Culture is difficult and hazardous (need tissue culture and eggs)
Diagnosis • PCR is best (large hospitals); Enzyme assay for Ab production
• Avoid Weil-Felix agglutination test! Not specific for Rickettsia (proteus Ag).
Treatment • Tetracycline and Chloramphenicol.
Norris 5/30/15
Lyme Disease —> Borrelia burgdorferi
• Found in temperate zones mainly between latitudes 30˚N and 50˚N; a small
number of cases originate in southern hemisphere corresponding latitudes
Overview
(Australia, New Zealand).
• Spirochetes seen on Giemsa and Silver stains; microaerophilic.
• Tick (Ixodes; Lone Star Tick) carries sugar called α-Gal that humans do not
have —> also found in red meat, beef, pork, venison, rabbit, and some dairy
Red Meat products.
Allergy • When tick bites, it can trigger a person’s immune system to create antibodies to
the sugar that cause their body to reject red meat, setting off a serious allergic
reaction.
• Eggs hatch to larvae (spring to summer) —> larvae require a vertebrate blood
meal to develop into nymphs (early fall) —> nymphs become dormant in winter
Ixodes sp. Life
—> Require another blood meal to develop into adults (spring to summer —
Cycle Most infectious stage) —> adults mate and then lay eggs (summer to fall) —>
eggs remain dormant in winter.
• Borellia cells adhere to epithelial cells of a tick’s midgut and remain there
indefinitely in quasi-dormant state —> when tick feeds on mammalian or avian
B. burgdorferi host, microorganisms are exposed to higher temperature, which activates
(within tick) them —> activated organisms multiply, penetrate the gut wall, and spread
through the tick to its salivary glands —> from host salivary glands they are
injected into skin of host.
• Carried in small mammals such as mice —> Ixodes tick transmits from mice to
humans —> spirochetes disseminate systemically:
• Stage 1: (~10 days after bite) at inoculation site, bacteria multiply and migrate
outward —> generate a spreading annular red lesion surrounding clear bite
mark (Erythema Chronicum Magnum) in 40-50% of cases, flu-like symptoms.
Pathobiology • Stage 2: (weeks later) disseminated spirochetes proliferate —> inflammatory
response damages: CNS, heart, skin, joints —> secondary annular lesion
(Exanthem).
• Stage 3: (months to years) persistent —> inflammatory damage to joints, brain,
cardiomyopathy, and areas of skin atrophy (Acrodermatitis Chronicum
Atrophicans).
• B. burgdorferi in blood smear during early stage only.
Diagnosis • Serology for later stage is unreliable: ELISA, IFA.
• Skin biopsy: spirochete, motile under dark-field microscopy.
Treatment • Doxycycline or amoxicillin for Stage 1.
• Ceftriaxone or Cefotaxime for later stages with prolonged therapy.
Prevention • Proper barrier clothing; insect repellants; prompt removal of ticks (requires 24
hours to inject sufficient inoculum); prophylaxis with 200mg doxycycline in first 72
and Control
hours of bite.
 Zoonoses Norris 6/4/15

Viral Hemorrhagic Fever Syndrome Bunyaviruses

• Multisystem syndrome that can be severe and life threatening; damage to overall Overview • Genome: ss(-ve)RNA (3 segments:S,M,L).
vascular system; in severe cases accompanied by hemorrhage.
Overview • Four families implicated: Arena-, Bunya-, Flavi-, and Filoviridae. Epidemiology • Reservoir in rats, mice, ticks.
• No vaccines available for any of these (Ebola?)
• Diagnosis by serology and virus isolation or genome amplification by PCR. Pathogenesis • Plasma and RBCs leak through vascular epithelium

Summary of Hemorrhagic Fevers Hantaan Virus • Hemorrhagic fever with renal syndrome; mice/rats; far east, scandinavia, E. europe.
• Severe pulmonary syndrome in SW USA (Sin Nombre); No vaccines.
Family Genus Virus Disease Natural Vector Geography
Congo- • Incubation 1-14 days; characteristic 2 peak fever:
Lassa Lassa Fever West Africa Crimean • Phase 1: High fever (40˚C) and lasts for 10-12 days, with malaise, fatigue, body aches,
Arenaviridae Arenavirus Rodent Hemorrhagic muscle and joint pain that lasts for up to a week. Hemorrhages from day 3-7 (low fever).
New World New World Hemorrhagic Virus • Phase 2: 1-2 days following hemorrhages the fever comes back.
Americas
Arenaviridae Fever

Africa, Central Flavivirdiae Flavivirus

Nairovirus Crimean Congo Hemorrhagic Fever Tick
Asia
• Yellow fever: Hepatitis, jaundice.
Bunyaviridae Africa, Arabian Clinical • Dengue fever: Breakbone fever (flue-like + severe joint/muscle pain).
Phlebovirus Rift Valley Fever Mosquito
Peninsula Presentation • Dengue hemorrhagic fever: (dengue fever + hemorrhage, shock).
• St. Louis, Japanese Encephalitis Virus: Encephalitis
Hantavirus Haem. Fever with Renal Syndrome Rodent Africa, Europe

Dengue Fever, Dengue Asia, Africa, • Normal reservoir in monkeys, birds, or humans —> transmitted by mosquito bite —>
Dengue Mosquito
Hemorrhagic Fever, Shock Americas enters bloodstream with transient viremia —> infects:
• hepatocytes (yellow fever) —> necrosis —> hepatitis and jaundice.
Flaviviridae Flavivirus Asia, Tropical • macrophages (dengue fever) —> acute inflammation —> pigeons and pain
Yellow Fever Mosquito Pathogenesis
Americas mediators —> “breakbone fever”
• if second infection by different serotype —> antibodies against first serotype
Omsk Hemorrhagic Fever Tick Central Asia increase and cross-react to form immune complexes —> type III hypersensitivity —>
Dengue hemorrhagic fever.
Ebola Ebola Hemorrhagic Fever Unknown Africa
Filoviridae Filovirus
Marburg Marburg Hemorrhagic Fever Unknown Africa Diagnosis • WNV-specific IgM in CSF by ELISA.

Arenaviridiae Arenavirus Filoviridae Filovirus

Overview • ss(-ve)RNA virus (2 segments); host ribosomes in the virus; no function.

Epidemiology • Reservoir in rats; spreads through rat feces and urine; mortality ranges 10%-50%.
• Incubation period: 6-21 days // 80% asymptomatic.
• Reservoir in rodents —> spread to humans by contamination of food or water with animal
Pathobiology excretions (can be nosocomial) —> viremia —> gradual onset of hemorrhagic fever —>
internal bleeding at GIT and other organs —>with severe disease: encephalopathy, ARDS,
Presentation
hemorrhagic shock, deafness in survivors.
• ss(-ve) RNA virus, enveloped, long filamentous virus (glycoprotein is highly
glycosylated, preventing strong host antibody response).
Overview • Virus RNA polymerase stutters at specific locations, adding extra nucleotides, thereby
“editing” the new RNAs —> make previously unidentified proteins.
• Proteins produced by glycoprotein editing are associated with virulence.
Clinical
• Hemorrhagic fever

Diagnosis • Serology: Blood and CSF. • Transferred to humans by direct contact —> incubation period 2-21 days —> viremia
with fever, flu-like symptoms —> viral infection of almost all organs —> focal necrosis
Treatment • Ribavirin Pathogenesis and hemorrhagic manifestations (especially GI, renal systems) —> shock, multiorgan
failure —> high mortality 1-2 weeks after onset of symptoms.
• Venezuelan Hemorrhagic fever. • Transmitted to other humans via bodily fluids (BL4 pathogens).
Similar
• Similar symptoms; can be mistaken for Dengue and other hemorrhagic diseases.
species
Reservoir in cane and cotton rats; mortality 30-40%; no vaccine; rodent control to prevent. Diagnosis • Serology