What organism causes Cat Scratch Disease?
T/F Cat scratch disease is a serious, life threatening disease in all humans
FALSE Self limiting disease in immunocompetent hosts (no abx needed)
Lesions from B. henselae demonstrate _____ spread, and will cause a _____
Demonstrate lymphatic spread Will cause a regional lymphadenopathy
What is the manifestation of Cat Scratch disease (B. henselae) characterized by sepsis in immunocompromised patients?
Lesions of Bacillary Angiomatosis from B. henselae resemble _____, and must be distinguished by biopsy.
What sequelae of Cat Scratch disease (B. henselae) is characterized by the presence cystic, blood filled lesions in the liver and spleen parenchyma of immunocompromised patients? What are some other symptoms of this sequelae?
Hepatic or Splenic Peliosis
Other sx: Target organ enlargement, weight loss, nausea, fever, and elevated liver enzymes and alkaline phosphate.
How is Cat Scratch disease (B. henselae) diagnosed?
Serology and physical findings
The organism is hard to culture
How is bacillary angiomatosis and peliosis caused by B. henselae infection of immunocompromised patients treated?
B. henselae appears as a gram _____, slightly curved _____
B. henselae appears as a gram NEGATIVE, slightly curved ROD
The disease caused by Ehrlichia chaffeensis, Ehrlichia ewingii and Anaplasma phagocytophilum is similar to RMSF except that _____. What is the vector? What kind of cells do they infect? Tx?
Presents with NO rash and leukopenia/thrombocytopenia
Vector = ticks
They infect monocytes and granulocytes
Tx: Tetracycline or chlorampheniol
What organism(s) cause Human Monocytic Ehrlichosis (HME)? Human Granulocytic Ehrlichosis (HE)?
HME: E. chaffeensis
HE: E. wingii/A. phagocytophilum
T/F: HME and HE always presents as a self limiting disease
Depending on the severity (# of WBC infected), HME and HE can be fatal
Pasteurella multocida appears as a gram _____ _____
Gram negative rod
What are the two virulence factors of Pasteurella multocida?
1) Anti-phagocytic capsule
How is Pasteurella multocida transmitted?
Through bites/scratches from cats or dogs (found in their oral cavity)
Pasteurella multocida causes _____ within 1-2 days after a bite. It presents as _____ in COPD patients.
Cellulitis 1-2 days after bite
Chronic lung infection in COPD patients
How is Pasteurella multocida diagnosed? Tx?
Diagnosis: Routine culture
The polypeptide capsule of Bacillus anthracis is made of _____ and provides the organism with protection from _____
Made of D-glutamic acid
Protects B. anthracis from phagocytosis
What virulence factor of B. anthracis is immunoprotective, is a component of the anthrax vaccine, and is a common binding subunit for other toxins?
Protective Angiten (PA)
B. anthracis Edema Toxin causes cell swelling and burst? How does it accomplish this?
Edema Toxin is an adenylate cyclase that increases cAMP
What virulence factor of B. anthracis cleaves MAP kinase? What does this induce in the host?
Induces apoptosis and T cell proliferation
The virulence factors of B. anthracis are found _____ that are required for the organisms virulencs
Found on two plasmids. Both are required for virulence
T/F B. anthracis is an obligate aerobe
_____ of B. anthracis represent the resting stage of the organism. They are very very resistant to disenfectants.
What are the two forms of B. anthracis spores? How do they gain access to human hosts?
1) Respiratory Anthrax: Inhalation through mucous membranes
2) Cutaneous Anthrax: Entrance through breached skin
What is the first sign of cutaneous anthrax infection?
Papule (painless ulcer) w/ coal-black necrotic center
A failure of the papule of cutaneous anthrax to heal can result in _____, leading to _____
Lymphatic spread leading to bloodstream dissemination (5-20%) and septicemia/death
Another name for Inhalation anthrax is _____
The spores of B. anthracis germinate inside human _____
What are the initial symptoms of inhalation anthrax? What causes these syptoms
Sx: Fever, dry cough (non-secific sx similar to a cold or flu)
The death of infected macrophages causes the release of pro-inflammaroty cytokines that produce these symptoms
2-4 days after the initial symptoms of inhalation anthrax, ______ follows, leading to _____ within 24 hours. What happens because of these late stage events?
Initial symptoms > Massive toxemia (2-4 days later) > Respiratory distress/shock/death (within 24 hours)
The release of toxins causes massive pulmonary edema and mediastinal hemorraghe (100% fatal!)
How is B. anthracis diagnosed in the lab?
Gram stain of fluid/pus from lesion/blood/sputum
Reveals gram positive rods in chains
B. anthracis is a gram _____ _____ in the blood and/or CSF
Gram positive rod
T/F: B. anthracis appears as a non-motile, non-hemolytic organism on blood agar.
What is the characteristic X-ray finding of anthrax?
What are the two treatment options for anthrax?
Cipromycin or Doxycycline
_____ is a monoclonal antibody that blocks the binding of B. anthracis Protective Antigen. It prevents/reduces _____
A patient comes to you presenting with the symptoms of massive toxemia caused by the second stage of inhalation anthrax. What can you do for this patient?
Administer raxibacumab to reduce toxemia, but at this point most of the damage has been done. Abx will be ineffective, and the patient has a very high chance of dying.
What are the two adehsins expressed by Yersinia pestis?
1) pH 6 adhesin (pilus adhesin, maximally expressed at pH 6)
2) Yersinia adherence (YadA)
What are the three Yersinia outer membrane proteins (Yops)? What are their functions? How are these potent toxins introduced?
1) YopH: Tyrosine phosphatase activity interferes with intercellular signaling
2) YopM: Indirectly affects signaling, preventing platelet release of cytokines
3) YopE: Destroys actin monofilaments (cytoskeleton component)
All are introduced via Type III secretion (direct injection into target cell cytoplasm)
What virulence factor of Y. pestis functions as the "Yops master switch", making it essential for their full expression?
LvrV (V antigen)
What Y. pestis virulence factor is an anti-phagocytic *protein* capsule that also activates complement?
Fraction 1 (Fra. 1)
What virulence factor of Y. pestis degrades C3b and C5a, Yops, and fibrin clots? What do these functions accomplish?
Degradation of Yops prevents immune system notice of the organism
Dissolution of fibrin clots makes it a spreading factor (its main function)
What disease caused by Y. pestis 1) has person to person transmission and is still survivable. Which one 2) is trasmitted person to person via the respiratory route, and is the "best" form to cause disease?
1) Bubonic plague
2) Pneumonic plague
Where does Y. pestis replicate?
Draining lymph nodes (access via lymphatic spread after flea bite)
A _____ is an inflamed/enlarged lymph node that has become hemorraghic from replication/infection by Y. pestis.
How does Y. pestis appear on staining of blood, sputum, or aspirates from buboes?
Gram negative rods w/ bipolar staining (safety pins)
How does Y. pestis appear on blood agar? Hint: it's a buzzword.
What are the two treatment options for Y. pestis?
What organism causes Rabbit Fever?
What are the four ways humans can acquire Rabbit Fever (F. tularensis)?
1) Handling skin/carcass of infected animals (rodents, beavers, etc.; carnivores who eat rodents, beavers etc.)
2) Insect vectors (ticks)
3) Animal bites
4) Inhalation causing pneumonia
T/F F. tularensis is a minimally invasive species
F. tularensis is VERY invasive
What tissues can F. tularensis infect?
Anything with a mucous membrane (Ulceroglandular, Glandular, Oculoglandular, Oropharyngeal infxns)
F. tularensis may become systemic (30-60% mortality) or pneumonic
T/F F. tularensis can't be cultured in the lab
Too dangerous for culture
How does F. tularensis appear on gram stain?
Gram negative rod
What are the two treatment options for Rabbit Fever (F. tularensis)?
F. tularensis, when transmitted by a tick/animal bite, causes a ______