1. Bartonella Classification

2. Species that most effect humans?

1. Short, Gram-, aerobic rods

2. B. bacilliformus, B. henselae, B. quintana

- Causes carrion disease, an acute     febrile illness, with severe anemia and chronic cutaneous form.

-Infection via sandfly bite in Andes

-Bacteria penetrates erythrocytes and makes the cells fragile and susceptible to clearance.

-Chronic stage consist of cutaneous nodules engorged in blood lasting months to years

-Caused trench fever during WWI

-Severe headaches, fever, weakness, and pain in long bones, can cause vascular lesions

-Can occur in five day intervals (5-day fever)

-Exposure to contaminated feces of human Louse is main cause of spread

-Causes bacteremia and bacillary angiomatosis in HIV+ patients.

-causes bacillary angiomatosis and subacute endocarditis but primarily involves the skin, lymph nodes, liver, or spleen

-Reservoirs are cats and their fleas, carried asymptomatically. 

-Causes cat scratch disease in children causing chronic regional adenopathy 

-Can only be collected from the blood in an immunocompromised patient. No cultures can be made on healthy individuals

Treatments for Bartonella

1. Bacilliformis

2. Cat Scratch Fever

3. In HV patients

1. Bacilliformis- Chlorophenicol, doxycycline, or rifampin.

2. Cat Scratch Fever- azithromycin

3. In HV patients- azithyromycin or clarithromycin

-Small gram(-) Rods, but stain poorly with gram stain

-Only grow in cytoplasm of eukaryotic cells

-Transmitted through arthropod vectors

-Subdivided into spotted fever group and typhus group 

-Transovarian transmission occurs in arthropods

-No flagella and is surrounded by a slime layer

-Enter hosts by binding to cell surface receptors and signaling for phagocytosis, then degrades phagosome and is released into the cytoplasm

-Able to make their own ATP via the tricarboxylic acid cycle

R. rickettsii

Pathogenesis and Epidemiology

-Causes rocky mountain spotted fever

-Protein A (Omp A) binds to surface of endothelial cells.

-Multiple in cytoplasm and nucleus 

-Cause leaking in the endothelial cells

-Caused by tick bites in the US

-Blood activates the bacteria in the tick and releases into the human blood

-Symptoms develop 7 days after bite

-malaise, myalgias, nausea, vomiting, abdominal pain, diarrhea, and a macular rash. 

R. rickettsiae

Diagnosis and Treatment

-Spotted fever group

-Because it does not stain well with Gram stain, Giemsa stain is required

-Antibody is a commonly used diagnosis

-PCR testing for protein A

-Culture on embryonated eggs

-Doxycycline is the drug of choice

-No available vaccine

-Spotted fever group

-Causes Rickettsialpox

-Cosmopolitan distribution and is transmitted by infected mites

-Biphasic Infection

   1. Papule develops at the site of the bite then         turns into an eschar

   2. Fever, headache, chills, sweats, and                   photophobia develop after 7-24 days and a         pox like rash forms after 3 days

-No medication needed

-Typhus group

-Causes louse born Typhus

-Present is third world areas with common lyse infections

-Flying Squirrel may be the vector in the US but not common

-Disease can occur years after the bite occurs

-Symptoms include fever, headache, and myalgias

-Disease may last 2 weeks- 3 months

-Tetracyclines are drugs of choice, but louse control methods must also be used

-Typhus group

-Causes endemic or murine typhus

-Lives mainly in warm humid areas

-Rodents are the primary reservoirs, and rat flea is the vector

-Symptoms appear 7-14 days after bite

-Include fever, severe headache, chills, myalgias, nausea, and rash in about 50%.

-IFA test confirms diagnosis

-Tetracyclines are the drug of choice

-Gram(-) rods, lacks peptidoglycan layer and LPS

-Enters the cell by phagocytosis

-Scrub Typhus

-Transmitted to humans by mites

-infects people living in Asia, Australia, and Japan

-6-18 day incubation period

-Headache, Fever, Myalgia

-Will go away on its own, but Doxyclycline will decrease recovery time

-Obligate intracellular bacteria 

-survive in cytoplasmic vacuoles

-Parasitize granulocytes, monocytes, erythrocytes, and platelets

-Remain in vacuole but prevent binding to a lysosome but stopping expression of certain receptors

-Two Morphologic Forms

   1. elementary bodies 

   2. reticulate bodies

-After infection reticulate bodies form into morulae detected by Giemsa Stain

-Similar to gram(-) but lack LPS and peptidoglycan

-Doxycycline is drug of choice

-Causes Human Monocytic Ehrlichiosis

-Infection of Blood monocytes and mononuclear Phagocytes in tissue and organs

-Flulike symptoms

-Rash in 30-40%

-Leukopenia, Thrombocytopenia, and elevated serum transaminase

-Very few infected cells cause big problems

-Immune system causes lots of the problems

-Lone Star Tick is the Primary vector

-White Tail Deer is Primary Reservoir

Coxiella Burnetii

Structure and Pathogenesis

-Gram(-), but stain weakly

-Grow intracellularly

-Causes Q fever

-Two Variants: Small Cell and Large Cell

-Small cell are phagocytosed and rearranged into Large cell then replicate, then turn back into the small cell and are released

-Contains a phase I antigen that blocks antibody interaction

-Mutation occurs and makes a phase II antigen that are exposed to antibodies

C. burnetii

Epidemiology and Clinical Course

-Can survive in soil and milk for months to years

-Farm animals are the primary reservoirs 

-Human infection occurs after inhalation of airborn pathogens released from feces or from unpasteurized milk

-Most people are asymptomatic

-Some have flulike symptoms

-Subacute endocarditis can occur in chronic Q fever

-Serologic test are now the standard

-Doxycycline is the standard

-Vaccination is available (single dose)