Download chapter 36 - Lange Textbooks

CHAPTER 36
Plague and Other Bacterial Zoonotic Diseases
Many bacterial, rickettsial, and viral diseases are classified as zoonoses, because they are
acquired by humans either directly or indirectly from animals. This chapter considers
bacteria causing four zoonotic infections that are not discussed in other chapters. All four
species, Brucella, Yersinia pestis, Francisella tularensis, and Pasteurella multocida, are
Gram-negative bacilli that are primarily animal pathogens. The diseases they cause,
brucellosis, plague, tularemia, and pasteurellosis, are now rare in humans and develop
only after unique animal contact.
BRUCELLA
I. BACTERIOLOGY
1. Coccobacilli resemble Haemophilus
2. Although long assigned to multiple species the three most common in humans
(B. abortus, B. melitensis, B. suis) are now considered variants of Brucella
abortus
3. Growth is slow, requiring at least 2 to 3 days of aerobic incubation
II. BRUCELLOSIS
A. EPIDEMIOLOGY
1. Brucellosis, a chronic infection that persists for life in animals
2. Causes abortion in cattle, goats, pigs
3. Humans acquire brucellosis by occupational exposure or consumption of
unpasteurized dairy products
4. Occupational disease for veterinarians
5. Unpasteurized dairy products and "health" foods are a risk
B. PATHOGENESIS
1. Brucella are facultative intracellular parasites of epithelial cells and
professional phagocytes
2. Inhibits myeloperoxidase, lysosome fusion and apoptosis
3. Multiplies in endoplasmic reticulum vesicles
4. Animal placental erythritol stimulates growth
5. Human infection forms granulomas in the reticuloendothelial sites with release
of bacteria into the blood
C. IMMUNITY
1. Macrophage killing requires Th 1-type responses
III. BRUCELLOSIS: CLINICAL ASPECTS
A. MANIFESTATIONS
1. Brucellosis starts with malaise, chills, and fever 7 to 21 days after infection
2. Pattern of periodic nocturnal fever (undulant fever) typically continues for weeks,
months, or even 1 to 2 years
3. Recurrent bacteremia comes from reticuloendothelial sites
4. Night sweats and periodic fever continue without obvious organ focus
B. DIAGNOSIS
1. Blood culture is primary method
2. Serologic tests may be useful
C. TREATMENT AND PREVENTION
1. Doxycycline plus aminoglycoside is effective
2. Pasteurization of dairy products is primary prevention
YERSINIA PESTIS
I. BACTERIOLOGY
1. Member of the Enterobacteriaceae and shares features of the other Yersinia
pathogenic for humans (Y. pseudotuberculosis, Y. enterocolitica)
2. Virulence plasmids, which code for a glycoprotein capsular antigen called F1 and
enzymes with phospholipase, protease, fibrinolytic and plasminogen activating
activity
3. Yersinia outer membrane proteins (Yops), protein capsule, and enzymes are
present
II. PLAGUE
A. EPIDEMIOLOGY
1. Y. pestis was the cause of the most virulent epidemic plague of recorded
human history, the Black Death of the Middle Ages
2. Plague is a disease of rodents transmitted by the bite of rat fleas (Xenopsylla
cheopis) that colonize them
3. Sylvatic transmission among wild rodents is primary reservoir
4. Rat migration to cities increases human risk
5. When infected rodents enter a city, circumstances for a cycle involving urban
rats are created
6. Fleas regurgitate into bite wounds
7. The bite of the flea is the first event in the development of a case of bubonic
plague
8. Some patients with bubonic plague develop a secondary pneumonia by
bacteremic spread to the lungs causing pneumonic plague
9. Pneumonic plague is contagious
10. Nonepidemic disease is linked to direct animal contact
11. Most US cases are in arid western states
B. PATHOGENESIS
1. Of the more than 20 known virulence factors some are deployed primarily in
the flea while others are produced only in the rodent or human victim
2. Y. pestis has regulatory systems which sense temperature, calcium, and surely
other environmental triggers in order to turn the production of appropriate
virulence factors on or off
3. Multiplication in flea foregut is aided by low temperature virulence factors
4. In a warm-blooded host F1 protein, Pla, Yops produced at 37oC
5. F1 is antiphagocytic
6. Yops destroy and disrupt host cells
7. Bubo progresses to bacteremia
8. LPS and other products produce shock
C. IMMUNITY
1. Anticapsular antibody may be protective
III. PLAGUE: CLINICAL ASPECTS
A. MANIFESTATIONS
1. Onset is marked by fever and the painful bubo, usually in the groin or, less often,
in the axilla
2. Pneumonic plague begins with fever, malaise. Cough, production of sputum,
dyspnea, and cyanosis develop in a few days
3. Bubonic plague mortality is 50–75% in untreated cases
4. Pneumonic plague is fatal if untreated
5. Terminal cyanosis = Black Death
B. DIAGNOSIS
1. Immunofluorescent staining is rapid
2. Cultures grow on routine media
C. TREATMENT
1. Streptomycin or gentamicin primary treatment
D. PREVENTION
1. Avoid sick or dead wild rodents
2. Chemoprophylaxis with doxycycline or ciprofloxacin for respiratory exposure
FRANCISELLA
I. BACTERIOLOGY
1. Gram-negative coccobacilli have growth requirement for –SH compounds
II. TULAREMIA
A. EPIDEMIOLOGY
1. Infecting dose is low
2. Acquired by tick bites or directly from wild mammal
3. Distributed throughout Northern Hemisphere
B. PATHOGENESIS
1. Intracellular multiplication is key to virulence
2. Escapes phagosome to cytosol
C. IMMUNITY
1. Cell-mediated immunity is dominant
III. TULAREMIA: CLINICAL ASPECTS
A. MANIFESTATIONS
1. Ulceroglandular, oculoglandular, typhoidal, and pneumonic forms exist
2. Ulceroglandular has lowest mortality
B. DIAGNOSIS
1. Special media are needed for culture
2. Serodiagnosis is most common
C. TREATMENT AND PREVENTION
1. Aminoglycosides are effective
PASTEURELLA MULTOCIDA
1. P. multocida, one of many species of Pasteurella in the respiratory flora of
animals Infections are treated with penicillin.
2. Penicillin-sensitive, Gram-negative rods
3. Most common cause of infected domestic animal bites or scratches