ZOONOTIC INFECTIONS
ZOONOTIC INFECTIONS
All REPORTABLE diseases
BACILLUS ANTHRACIS: Gram(+) large rods with square ends.
Name-Derivation: Anthracis = of sheep, cattle.
Epidemiology / At Risk:
Cutaneous = 95% of infections.
Inhalation = 5%
Ingestion is not seen in the United States.
Manifestations: ANTHRAX.
CUTANEOUS: Black Eschar, found on head, hands, forearms.
Erythema and induration, but no pus. Any pus present would be a secondary bacterial infection.
PULMONARY: Wool-Sorter's Disease. Wool-spinners are at risk.
Inhaled spores are phagocytosed by alveolar macrophages. Replication occurs in macrophage, then macrophage travels to lymph nodes where it disseminates.
Fever, edema, and death within 24 hours from toxemia.
Ingestion: Dysentery followed by shock and death; not seen in USA.
Processing:
Specimen: Aspirate of blister (eschar) fluid.
Stain:
Gram-stain would show large rods, with squared end and no capsule.
Methylene Blue, Giemsa stain is required to see the thin capsule.
Culture:
It yields ROUGH colonies with no zone of hemolysis.
The capsule is not grown in vitro (conditions are not right), so that they have attenuated virulence.
Identification:
Bacillus genus is identified by rough, medusa-head colonies.
SPECIES:
PENICILLIN: Anthracis species is identified by a String of Pearls formation in penicillin. The colonies are susceptible to penicillin, whereas other Bacillus species are not.
gamma-PHAGE: Will attack and lyse Anthracis on a plate, but not other Bacilli.
Can also do a Fluorescent Antibody of the cell-wall polysaccharide can be done -- but not the capsule, because the capsule isn't present in vitro!
Virulence:
Cell-Associated:
CAPSULE: It is composed of protein -- poly-d-Glutamic acid -- not polysaccharide.
Antigenic and antiphagocytic.
Plasmid-Mediated property, thus we can manipulate it for vaccine use.
Cell-Wall Polysaccharide: Composed of N-Acetylglucosamine and d-Galactose.
It cross-reacts with the Group-A blood type.
Can be used in lab for ID.
Exotoxin: ANTHRAX TOXIN is a plasma-mediated, heat-labile toxin. It has three components.
Protective Antigen: Binds to surface receptor. It is antigenic, and host-response yields protective antibodies (protective against toxin -- not against the bug).
Edema Factor: Bug-derived adenyl cyclase enters host cell ------> cAMP ------> electrolyte and water loss.
Lethal Factor: Metalloprotease enters and kills host cells. Mechanism unknown.
Host Immune Response: Antibodies to the capsule and polysaccharide are not protective. Antibody to toxin is protective.
Vaccine / Prevention:
CATTLE vaccine: Viable spores from an attenuated strain (they have no capsule), plus an alum precipitate (adjuvant) to improve immunogenicity.
Edema factor and Lethal factor are also removed.
Humans: Only at-risk people. We give alum precipitate plus the protective antigen alone. Multiple shots required.
Treatment: Penicillin.
BACILLUS CEREUS:
Epidemiology / At Risk:
Food-Poisoning = refried beans and rice
Bacteremia = OPPORTUNISTIC. Nosocomial, immunocompromised patients.
Manifestations:
Food-Poisoning in refried rice and beans is self-limiting to about 24 hrs.
Early on (1-6 hrs): Nausea and vomiting
Later (24 hrs): Profuse diarrhea
Bacteremia (contaminated catheters) in immunocompromised leads to meningitis, endocarditis, death.
Identification:
B. Cereus is penicillin-resistant. They will form chains of rods rather than string of pearls in penicillin suspension.
gamma-PHAGE does not lyse it.
Virulence:
Enterotoxins:
Emetic Toxin: Heat stable, basis for early symptoms.
Diarrheal Toxin: Heat labile, basis for late onset.
Stimulates host cell adenyl cyclase ------> cAMP
Chromosomal beta-Lactamase and Cephalosporinase
BACILLUS SUBTILIS:
Epidemiology / At Risk: Heroin preparations can be contaminated with it.
Manifestations: Environmental contaminant that can cause very destructive lesions associated with heroin use.
Identification: It is susceptible to penicillin.
FRANCISELLA TULARENSIS: Gram(-) rod.
Name-Derivation: Named after who and where it was discovered.
Epidemiology / At Risk:
Endemic to SE Kansas, carried by small mammals (via ticks).
Fewer than 50 organisms can cause a full infection!
Manifestations: The bug is a facultative intracellular parasite of macrophages.
Initial infection ------> PMN's can't kill it ------> macrophages phagocytize it but don't kill it ------> travel to lymph nodes ------> very painful, suppurative infection of lymph nodes.
Lymph node clearance may take up to a year. Anorexia is common during this time.
Processing:
Stain: Short-rods that are faintly gram-negative. Incorrectly referred to as "coccobacilli."
Giemsa: Short-rods that stain more intensely at the poles.
Fluorescent Antibody to capsular antigen is available in Kansas.
Culture: CYSTEINE-AGAR must be used. Must communicate with the lab what you're looking for!
CO2 is also required for growth.
Growth takes up to 3 days -- longer time than usual.
Identification:
Smooth, gray colony on culture.
Antibody agglutination test to most virulent Strain A, which is endemic to Kansas.
SEROLOGY: Collect an early and late specimen
Early would show 1:40 Ab titer, as Francisella cross-reacts with Yersinia antibodies.
Late would show 1:320 titer -- 4X difference minimum to be significant.
Virulence:
Intracellular Parasite of macrophages. This is most important property.
Capsule: Polysaccharide is antiphagocytic and confers serum resistance.
Patient hypersensitivity to this polysaccharide will remain for years. Skin-tests can be done.
Host Immune Response:
Activated (IL-2, cell-mediated) macrophages are necessary for protection. They can kill the organism.
Delayed hypersensitivity develops to cell wall antigens.
Vaccine / Prevention: Live attenuated organism is used. Patient will develop antibody and delayed hypersensitivity.
Only used on lab workers.
YERSINIA PESTIS: Gram(-) rod.
Epidemiology / At Risk: Rats and fleas.
SYLVATIC CYCLE: Infection cycle between carrier rodents and fleas.
URBAN CYCLE: New Yersinia strain kills large numbers of rats, and fleas spread the infection via dead rat carcasses.
BUBONIC CYCLE: Begins when fleas spread the bug to humans.
Bacteria reproduce in flea to the point where they clog the proventriculus. Human bite ------> inoculation of bacteria into host.
Manifestations: PLAGUE
BUBONIC FORM: Flea bite.
Bite become indurated and necrotic.
Buboes (swollen lymph node) results from initial flea bite.
Bugs undergo large temperature increase from 25C to 37C, which initiates new virulence properties (YOP's and F1 antigen).
High fever, bacteremia, pneumonia, sepsis.
PNEUMONIC FORM: Inhalation of aerosolized droplets spread by human to human contact (coughing).
Fever, malaise, pulmonary edema, death within 24 hrs.
Processing:
Specimen:
Lymph node aspirate (painful) for bubonic form. Inject saline into lymph node and then withdraw saline.
Pneumonic Form: blood, sputum, or lymph node.
Special transport medium is necessary for transfer to protect handlers.
Stain: No gram stain.
Wayson's stain shows a short rod.
Culture: Must advise lab.
Specimen held at 28C to reduce virulence.
Smooth brownish colonies.
Iron is required for growth.
Identification:
Agglutination test against F1 Capsular-protein
SEROLOGY: F1-Antibody Test after 5 days is diagnostic of plague.
Group classification is made based on the characteristics of the YOP's.
Virulence: Plasmid-regulated. The factors themselves are on the chromosome, but the regulatory operons are on plasmids.
REGULATION: The plasmid is activated by signals that come from temperature change of 25C to 37C.
FLEA: Coagulase is produced at 25C, which entraps the bug in fibrinous material in the flea. This is how the proventriculus gets clogged, which leads to the flea regurgitation into humans.
HUMAN Virulence: All of these factors are activated at 37C. Order of events (first line of defense, second line).
Fibrinolysin is produced at 37C, to dissolve the clot.
F1 Antigen (Envelope): Antiphagocytic and antigenic. Ab is made but it is not protective.
The bugs multiply like crazy. PMN's can't handle the sheer number of bugs, so macrophages come along as second line of defense.
pH 6 Antigen allows the bug to survive inside the phagolysosomes of blood macrophages.
Yersinia Outer Proteins (YOP's): V & W proteins are produced. They allow replication inside fixed macrophages in liver and spleen
YOP's are also antiphagocytic for PMN's.
Other factors: Siderophore (iron) and an endotoxin that promotes fever.
Host Immune Response:
Antibody to the F1 antigen promotes opsonization, but killing is not effective.
Activated macrophages (CMI) are required to kill the bug.
Vaccine / Prevention: Quarantine is required. Rat control to prevent infection.
Treatment: Streptomycin + Tetracycline. Tetracycline used prophylactically for at risk folks.
All REPORTABLE diseases
BACILLUS ANTHRACIS: Gram(+) large rods with square ends.
Name-Derivation: Anthracis = of sheep, cattle.
Epidemiology / At Risk:
Cutaneous = 95% of infections.
Inhalation = 5%
Ingestion is not seen in the United States.
Manifestations: ANTHRAX.
CUTANEOUS: Black Eschar, found on head, hands, forearms.
Erythema and induration, but no pus. Any pus present would be a secondary bacterial infection.
PULMONARY: Wool-Sorter's Disease. Wool-spinners are at risk.
Inhaled spores are phagocytosed by alveolar macrophages. Replication occurs in macrophage, then macrophage travels to lymph nodes where it disseminates.
Fever, edema, and death within 24 hours from toxemia.
Ingestion: Dysentery followed by shock and death; not seen in USA.
Processing:
Specimen: Aspirate of blister (eschar) fluid.
Stain:
Gram-stain would show large rods, with squared end and no capsule.
Methylene Blue, Giemsa stain is required to see the thin capsule.
Culture:
It yields ROUGH colonies with no zone of hemolysis.
The capsule is not grown in vitro (conditions are not right), so that they have attenuated virulence.
Identification:
Bacillus genus is identified by rough, medusa-head colonies.
SPECIES:
PENICILLIN: Anthracis species is identified by a String of Pearls formation in penicillin. The colonies are susceptible to penicillin, whereas other Bacillus species are not.
gamma-PHAGE: Will attack and lyse Anthracis on a plate, but not other Bacilli.
Can also do a Fluorescent Antibody of the cell-wall polysaccharide can be done -- but not the capsule, because the capsule isn't present in vitro!
Virulence:
Cell-Associated:
CAPSULE: It is composed of protein -- poly-d-Glutamic acid -- not polysaccharide.
Antigenic and antiphagocytic.
Plasmid-Mediated property, thus we can manipulate it for vaccine use.
Cell-Wall Polysaccharide: Composed of N-Acetylglucosamine and d-Galactose.
It cross-reacts with the Group-A blood type.
Can be used in lab for ID.
Exotoxin: ANTHRAX TOXIN is a plasma-mediated, heat-labile toxin. It has three components.
Protective Antigen: Binds to surface receptor. It is antigenic, and host-response yields protective antibodies (protective against toxin -- not against the bug).
Edema Factor: Bug-derived adenyl cyclase enters host cell ------> cAMP ------> electrolyte and water loss.
Lethal Factor: Metalloprotease enters and kills host cells. Mechanism unknown.
Host Immune Response: Antibodies to the capsule and polysaccharide are not protective. Antibody to toxin is protective.
Vaccine / Prevention:
CATTLE vaccine: Viable spores from an attenuated strain (they have no capsule), plus an alum precipitate (adjuvant) to improve immunogenicity.
Edema factor and Lethal factor are also removed.
Humans: Only at-risk people. We give alum precipitate plus the protective antigen alone. Multiple shots required.
Treatment: Penicillin.
BACILLUS CEREUS:
Epidemiology / At Risk:
Food-Poisoning = refried beans and rice
Bacteremia = OPPORTUNISTIC. Nosocomial, immunocompromised patients.
Manifestations:
Food-Poisoning in refried rice and beans is self-limiting to about 24 hrs.
Early on (1-6 hrs): Nausea and vomiting
Later (24 hrs): Profuse diarrhea
Bacteremia (contaminated catheters) in immunocompromised leads to meningitis, endocarditis, death.
Identification:
B. Cereus is penicillin-resistant. They will form chains of rods rather than string of pearls in penicillin suspension.
gamma-PHAGE does not lyse it.
Virulence:
Enterotoxins:
Emetic Toxin: Heat stable, basis for early symptoms.
Diarrheal Toxin: Heat labile, basis for late onset.
Stimulates host cell adenyl cyclase ------> cAMP
Chromosomal beta-Lactamase and Cephalosporinase
BACILLUS SUBTILIS:
Epidemiology / At Risk: Heroin preparations can be contaminated with it.
Manifestations: Environmental contaminant that can cause very destructive lesions associated with heroin use.
Identification: It is susceptible to penicillin.
FRANCISELLA TULARENSIS: Gram(-) rod.
Name-Derivation: Named after who and where it was discovered.
Epidemiology / At Risk:
Endemic to SE Kansas, carried by small mammals (via ticks).
Fewer than 50 organisms can cause a full infection!
Manifestations: The bug is a facultative intracellular parasite of macrophages.
Initial infection ------> PMN's can't kill it ------> macrophages phagocytize it but don't kill it ------> travel to lymph nodes ------> very painful, suppurative infection of lymph nodes.
Lymph node clearance may take up to a year. Anorexia is common during this time.
Processing:
Stain: Short-rods that are faintly gram-negative. Incorrectly referred to as "coccobacilli."
Giemsa: Short-rods that stain more intensely at the poles.
Fluorescent Antibody to capsular antigen is available in Kansas.
Culture: CYSTEINE-AGAR must be used. Must communicate with the lab what you're looking for!
CO2 is also required for growth.
Growth takes up to 3 days -- longer time than usual.
Identification:
Smooth, gray colony on culture.
Antibody agglutination test to most virulent Strain A, which is endemic to Kansas.
SEROLOGY: Collect an early and late specimen
Early would show 1:40 Ab titer, as Francisella cross-reacts with Yersinia antibodies.
Late would show 1:320 titer -- 4X difference minimum to be significant.
Virulence:
Intracellular Parasite of macrophages. This is most important property.
Capsule: Polysaccharide is antiphagocytic and confers serum resistance.
Patient hypersensitivity to this polysaccharide will remain for years. Skin-tests can be done.
Host Immune Response:
Activated (IL-2, cell-mediated) macrophages are necessary for protection. They can kill the organism.
Delayed hypersensitivity develops to cell wall antigens.
Vaccine / Prevention: Live attenuated organism is used. Patient will develop antibody and delayed hypersensitivity.
Only used on lab workers.
YERSINIA PESTIS: Gram(-) rod.
Epidemiology / At Risk: Rats and fleas.
SYLVATIC CYCLE: Infection cycle between carrier rodents and fleas.
URBAN CYCLE: New Yersinia strain kills large numbers of rats, and fleas spread the infection via dead rat carcasses.
BUBONIC CYCLE: Begins when fleas spread the bug to humans.
Bacteria reproduce in flea to the point where they clog the proventriculus. Human bite ------> inoculation of bacteria into host.
Manifestations: PLAGUE
BUBONIC FORM: Flea bite.
Bite become indurated and necrotic.
Buboes (swollen lymph node) results from initial flea bite.
Bugs undergo large temperature increase from 25C to 37C, which initiates new virulence properties (YOP's and F1 antigen).
High fever, bacteremia, pneumonia, sepsis.
PNEUMONIC FORM: Inhalation of aerosolized droplets spread by human to human contact (coughing).
Fever, malaise, pulmonary edema, death within 24 hrs.
Processing:
Specimen:
Lymph node aspirate (painful) for bubonic form. Inject saline into lymph node and then withdraw saline.
Pneumonic Form: blood, sputum, or lymph node.
Special transport medium is necessary for transfer to protect handlers.
Stain: No gram stain.
Wayson's stain shows a short rod.
Culture: Must advise lab.
Specimen held at 28C to reduce virulence.
Smooth brownish colonies.
Iron is required for growth.
Identification:
Agglutination test against F1 Capsular-protein
SEROLOGY: F1-Antibody Test after 5 days is diagnostic of plague.
Group classification is made based on the characteristics of the YOP's.
Virulence: Plasmid-regulated. The factors themselves are on the chromosome, but the regulatory operons are on plasmids.
REGULATION: The plasmid is activated by signals that come from temperature change of 25C to 37C.
FLEA: Coagulase is produced at 25C, which entraps the bug in fibrinous material in the flea. This is how the proventriculus gets clogged, which leads to the flea regurgitation into humans.
HUMAN Virulence: All of these factors are activated at 37C. Order of events (first line of defense, second line).
Fibrinolysin is produced at 37C, to dissolve the clot.
F1 Antigen (Envelope): Antiphagocytic and antigenic. Ab is made but it is not protective.
The bugs multiply like crazy. PMN's can't handle the sheer number of bugs, so macrophages come along as second line of defense.
pH 6 Antigen allows the bug to survive inside the phagolysosomes of blood macrophages.
Yersinia Outer Proteins (YOP's): V & W proteins are produced. They allow replication inside fixed macrophages in liver and spleen
YOP's are also antiphagocytic for PMN's.
Other factors: Siderophore (iron) and an endotoxin that promotes fever.
Host Immune Response:
Antibody to the F1 antigen promotes opsonization, but killing is not effective.
Activated macrophages (CMI) are required to kill the bug.
Vaccine / Prevention: Quarantine is required. Rat control to prevent infection.
Treatment: Streptomycin + Tetracycline. Tetracycline used prophylactically for at risk folks.
