animals

1. Zoonotic Diseases
Dr.Fatima Fasih
Associate Professor of Pathology
Section Head TB lab DDRRL

2. Lecture Objectives.
The students should be able to
• List and describe the common zoonotic infections
with reference to the mode of transmission and
pathogenesis.
• Know relevant diagnostic tests for these infections
• Demonstrate their knowledge for the preventive
measures and control of zoonotic infections.

3. Characteristics of zoonotic diseases
• All of the zoonotic diseases have one thing in common; the
animal reservoir.
• Humans are usually an accidental or dead end host.
Entry:
• Bite of an arthropod vector or an animal .
• Inhalation of contaminated materials or animal droppings
• Ingestion of food.

4. Mode of transmission
Spread
• All of these infections spread from the initial site
of inoculation and become systemic to varying
degrees.
Multiplication
• Most are fastidious and require special media,
the rickettsia require tissue culture.
• Most are intracellular pathogens, and many are
intracellular pathogens of phagocytes

5. Pathogensis
• Damage - inflammation, intracellular
cytotoxicity and sometimes exotoxins

6. Plague

7. Plague
Yersinia pestis
• A Non-motile gram-negative aerobic rod
that exhibits bipolar staining with special
stain.
• One of the most virulent bacteria known
(ID ,very low.1-10 organisms).
• Polysaccharide protein capsule, an
important virulence factor.

8. Etiology and Epidemiology
• Rat flea, Xenopsylla-cheopis is reservoir and
vector.
• Transmission is either through bites of
infected fleas from wild animals rodents
(sylavatic plague) or rats (urban plague).
• Or person to person through respiratory
aerosols.
• Endemic areas in the United States focus
around the western states

9. Pathogenesis
• Virulence factors include a protein capsule,
endotoxin, plasminogen activator protease,
and a series of YOPS proteins
• The organisms migrate from the site of flea
bite to regional lymph nodes (bubonic
plague).
• Invade blood stream (septicemic plague).
• Invasion of lungs (pneumonic plague).
• DIC and hemorrhage.

10. Clinical Sign/Symptoms
• Three major forms
• Bubonic plague is characterized by high fever
and large swollen inguinal, axillary, or cervical
lymph nodes called bubos. Progression can
result in a bacteremic phase with sudden
onset of fever and chills.

11. Clinical Sign/Symptoms
• Pneumonic plague results from inhalation of
infectious aerosols or embolization of
bacteremic organisms to the lung. Disease
development is rapid and highly fatal.
• Septicemic plague (black death) results from
endotoxin effects including necrosis of
peripheral blood vessels and disseminated
intravascular coagulation.

12. Clinical Sign/Symptoms
• Enlarged tender lymph nodes (buboes) in the
neck armpits and groin.
• Intense fever with septicemia.
• Terminal pneumonia
• Meningitis
• Heart /respiratory failure.

13. Lab. Diagnosis
• If plague is suspected, the laboratory
should be notified.
• Direct examination after staining and
culture from blood, sputum, or buboe
aspirate aids in diagnosis.

14. Lab. Diagnosis
• Blood, pus or aspirate from the bubo is taken
as sample and examined.
• High risk sample.
• Giemsa / Wayson’s staining shows typical
safety pin appearance.
• Fluorescent AB test.
• Serological test .Rise in AB titer for envelop.

15. Morphology

16. Treatment & Prevention
• The antibiotic of choice is streptomycin.
• Gentamicin, tetracycline, or chloramphenicol are alternatives
• Prevention involves avoidance of handling dead animals in
endemic areas and controlling rat populations in urban areas
• Strict isolation (Quarantine) for patients for at least 72 hours
after starting the treatment.
• An inactivated whole-cell vaccine is available for high-risk
individuals.

17. Tularemia
Francisella tularensis
• Small gram-negative cocco bacillus.
• Causes Tularemia (Rabbit Fever)

18. Etiology and Epidemiology
• This highly infectious organism is endemic to
many areas of the United States including
Arkansas,Missouri, and Oklahoma.
• Infection results from bites from infected ticks,
infectious aerosols, and contact with infected
tissues or body fluid of an infected animal.
• The infectious dose is around 50 organisms.

19. Clinical Manifestations
• A variety of disease manifestations include
ulceroglandular disease, oculoglandular
conjunctivitis, glandular disease, typhoidal disease,
and pneumonic.
• Influenza-like syndrome with fever
• Forms ulceroglandular ulcer at inoculation, lymph
adenopathy at regional nodes

20. Pathogenesis
• Two primary virulence factors include an
antiphagocytic capsule and endotoxin. F
tularensis can survive in cells of the
reticuloendothelial system
• Spread - from the site of inoculation into the
regional lymph nodes
• Evasion of defenses/multiplication, multiply in
macrophages

21. LAB Diagnosis
• Diagnosis is facilitated using flurorescent
antibody assays on clinical specimens and
serologic assays to detect specific antibody.
• The organism is slow growing and requires
special cysteine-rich media.
• Because it is highly infectious, laboratories
should be notified of suspected infections.

22. Treatment and Prevention
• F. tularensis is resistant to all beta-lactam antibiotics.
Antibiotics such as streptomycin or gentamicin
• Prevention involves avoidance of infected animals, aerosols,
and tick vectors
• Use insect repellents containing 20% to 30% DEET (N,N-
diethyl-meta-toluamide), picaridin or IR3535
• Wear long pants, long sleeves, and long socks to keep ticks
and deer flies off your skin.
• Remove attached ticks promptly with fine-tipped tweezers.

23. Lyme disease
Borrelia burgdorferi
• Lyme disease is caused
by the bacterium Gram-
negative spirochete
Borrelia burgdorferi
• Borrelia burgdorferi is
transmitted to humans
through the bite of
infected blacklegged
ticks.

24. Etiology and Epidemiology
• Transmission from small mammal reservoirs
occurs from bites of soft-bodied tick.
• Deer tick bite; nymphal stage (very small)
more likely than adult.
• Mice are immediate reservoir, but deer are
essential for tick life cycle
• Prolonged exposure (24–48 hours) is required
for efficient transmission.

25. Clinical Manifestations
• Causative agent of Lyme disease.
• Stage 1 disease: Early infection 3 - 30 days
after bite is characterized by a bull’s-eye rash
(erythema migrans) with a clear center that
may be accompanied by fever, chills, and
myalgia.
• Stage 2 disease occurs weeks to months later
with manifestations that may include limb
numbness, Bell’s palsy, meningitis,
encephalitis, and myocarditis.

26. Clinical Manifestations

27. Clinical Manifestations
• Stage 3- Latent stage
• Stage 4- chronic - chronic skin, nervous
system, or joint involvement. Arthritis of large
joints; also chronic progressive neurological
disease; immune response to persistent
bacterial antigens?
• Stage 5- Autoimmunity .

29. Cat Bite Fever
Pasteurella multocida

30. A Biphasic Illness
Leptospira interrogans
• Gram-negative spirochete

31. LEPTOSPIRA
1. Microbiology: spirochete, detected by dark
field microscopy.
2. Disease: biphasic illness:
a. First phase: bacteremic; 1 week
i. Nonspecific: fever, headache,
conjunctival suffusion, GI complaints,
myalgia, rash
ii. bloodstream  organs (liver, kidney) 
jaundice, hemorrhage, renal failure
iii. Resolution of fever - humoral
response (immune phase).

32. LEPTOSPIRA
b. Second phase: immune phase occurs
~2 days after the first phase; 1-4 weeks;
aseptic meningitis, conjunctivitis, diffuse
lymphadenopathy, hepatosplenomegaly.
c. Weil’s syndrome (icteric leptospirosis):
after first phase; triad: hemorrhage,
jaundice/hepatitis, renal failure. Creatinine
phosphokinas (CPK) extremely high due
to myositis.

33. 5
6. Damage:
a. Toxin - displaces long-chain fatty
acids from host endothelial cells ->
breakdown of blood vessel wall 
spirochete dissemination.
b. Thermolabile hemolysin.

34. 3. Diagnosis:
a. Culture of CSF, blood, urine – low yield
b. Dark field microscopy – (+) only during
early infection.
c. Serology: ELISA
4. Encounter/entry:
a. Ingestion or contact with contaminated
urine from infected domestic animals (dogs,
sheep, cattle, goat, sheep) or rats.
b. Broken skin and mucous membrane.
c. Occupational hazard for farmers,
veterinarians, hunters.

35. Rickettsia rickettsii
a. Disease - Rocky Mountain spotted fever
(mainly in eastern US), 100s of cases per year
in U.S.
b. Clinical manifestation
i. Acute onset of fever, headache, myalgia,
abdominal pain
ii. Rash (macular, petechial) begins on palms
and soles, ankles/wrists and spread to truck.
iii. Aseptic meningitis, conjunctivitis, ARDS.

36. Rickettsia rickettsii
c. Diagnosis –
i. Typical rash
ii. Immunofluorescent stain of skin/tissue
biopsy.
iii. serological test
iv. (old Weil-Felix test - detect cross-reactive
antibodies to Proteus).

38. d. Encounter/entry - wood tick and dog tick
from dogs or rodents; tick is both vector and
reservoir
e. Spread - causing vasculitis; actin
polymerization .
f. Multiplication - requires tissue culture.

39. g. Evades defenses - intracellular
h. Damage - 2 - 6 day incubation period;
infection of vascular endothelium resulting is
rash, hemorrhage, thrombosis, and edema
(macules progressing to petechial lesions)
rash spreads from hands and feet to trunk
(presence of rash on palms and soles - unique
characteristic); can be fatal if untreated.

40. Other Rickettsia:
(name recognition)
Rickettsia sp. Vector Disease
R. prowazekii Louse Louse-borne typhus (epidemic
typhus)
- rash: trunk spreading to
extremites; spares palms and
soles
R. typhi Flea Endemic (murine) typhus
- less severe than epidemic
typhus
R. tsutsugamushi Mite Scrub typhus
-similar clinically to epidemic
typhus

41. Ehrlichia (100s of cases/yr)
- transmitted by tick
- asymptomatic to fatal
- Classic presentation: fever, headache,
myalgia.
- Important lab test: thrombocytopenia,
leukopenia. <50% develop rash.
- Infects white blood cells.

42. Bartonella henselae
1. cat scratch disease
- benign local lymphadenopathy
2. bacillary angiomatosis (AIDS)
- proliferative vascular lesions in dermis
and internal organs

44. Brucella abortus
. Gram negative rod, coccobacillus
. Disease - Brucellosis (undulant fever, Malta
fever)
- very rare .
- fever, back or limb pain; splenomegaly
- long course (months)
Encounter - occupational exposure to infected animals
(ranchers, slaughterhouse, veterinarians), contaminated
milk; no arthropod vector

45. Entry - inhalation, ingestion, cuts in skin
. Multiplication, evade defenses - lives within
macrophages in reticuloendothelial system
(spleen, liver, lymph nodes, bone marrow), avoid
killing by PMNs; likes erythritol
Diagnosis - culture or serology

46. ACTINOMYCETES.
FILAMENTOUS GM+VE BACILLI.

47. ACTINOMYCETES.
• A gm +ve fungus like anaerobic bacillus. Some
are weakly acid fast.
• TRANSMISSION: Occurs in the normal flora of
upper respiratory &GI tract.It may invade
tissue after local trauma e.g tooth extraction
or broken jaw.

48. PATHOGENESIS.
• The bacteria enter gum tissue forming
filaments around which inflamation occurs.
Hard yellow granules(sulphur granules)
consisting of filaments are found in the pus.
• As it is an endogenous bacterium it can cause
infections of chest wall ,intestinal wall or
uterine wall.

49. CLINICAL S/S.
• Draining sinuses are formed in the tissue,may
grow in the facial muscle causing LUMPY JAW.
• Ulcers of chest or intestinal wall may occur.
• An I/u device left there for a long time can
lead to pelvic actinomycosis.

51. LAB.DIAGNOSIS.
• Isolation &identification of the organism can
be done by.
• gram+ve bacilli with branching filaments &
presence of sulphur granules.
• Culture of pus/tissue samples
ANAEROBICALLY.
• Immunofluoresense is also helpful in
diagnosis.

53. TREATMENT & PREVENTION.
• Penicillin G is the drug of choice,along with
surgical drainage.