Rickettsia and bartonella

Question 1

Rickettsiae transmission

Answer 1

obligate intracellular bacteria. They have animal reservoirs and are transmitted to humans by arthropod vectors such as lice, mites and fleas.

Question 2

rickettsia structure and visualization

Answer 2

gram-negative bacteria. Most frequently in pairs of rod-shaped cells with tapered ends, or as single coccobacilli. Stain poorly with bacteriologic stains, but they can be visualized readily in tissue with the Giemsa stain.

Question 3

Rickettsia growth

Answer 3

obligate intracellular (grow in cytoplasm). • Rickettsiae have efficient transport systems for acquiring ATP, amino acids, and other metabolites from the host cell. They are capable of independent metabolism (TCA cycle and electron transport system), and use their own biosynthetic machinery to make proteins and other complex components. However, they cannot be cultivated on artificial medium

Question 4

What cell does rickettsia infect

Answer 4

The bacteria invade the vascular endothelial cells and become widely disseminated throughout the vascular system. The pathology of rickettsial infections results from destruction of infected host cells.

Question 5

Rickettsial diseases- clinical features

Answer 5

fever, headache, and rash. The rash is due to focal areas of infection that cause increased vascular permeability and edema. Thrombosis and blockage of the small blood vessels with extravasation of blood are late events in pathogenesis. Petechial lesions are a hallmark of rickettsial diseases. The clinical consequences of lesions in the brain, kidneys, lungs, and heart are much greater than those of the cutaneous lesions.

Question 6

Compare the initial site of lesion in the three diseases cuased by Rickettsia and Orienta

Answer 6

Typhus group: rash appears first on the trunk and progresses to the extremities. Scrub Typhus group: rash is absent. Spotted fever group: rash appears first on the extremities, moves centripetally and involves the palms and soles

Question 7

List the diseases in the Typhus group

Answer 7

epidemic typhus, Brills disease, and endemic typhus

Question 8

Etiology/ transmission/ reservoirs of epidemic typhus

Answer 8

Rickettsia prowazekii. reservoirs in human and flying squirrels. • Transmission: Feces from human body louse and squirrel ecto-parasites. Prevalant during wars/ natural disasters

Question 9

Epidemic Typhus clinical features

Answer 9

Erythematous macular rash starting 1-2 weeks after inoculation. The rash starts on the trunk and progresses to the extremities. Bacteremia, high fever, prostration, renal failure, stupor. Up to 70% mortality untreated

Question 10

Epidemic Typhus prevention/ treatment

Answer 10

Live attenuated vaccine used in armed services and for people at risk. Insecticides to kill lice.
Treatment: Doxycycline.Live attenuated vaccine used in armed services and for people at risk. Insecticides to kill lice.
Treatment: Doxycycline.

Question 11

etiology of Brill’s disease

Answer 11

Rickettsia prowazekii

Question 12

Brills disease clinical features

Answer 12

• Similar to epidemic typhus except milder, usually no rash • Occurs many years after primary infection as a consequence of recrudescence, usually in immigrants from Eastern Europe who had typhus during World War II • If patients are infested with lice, there is a possibility of transmission • Brill’s disease can be the source of new outbreaks of epidemic typhus

Question 13

Endemic typhus etiology, reservoir, transmission

Answer 13

Rickettsia typhi. Reservoirs are rats. Transmission from feces of rat fleas.

Question 14

Endemic typhus clinical manifestations and treatment

Answer 14

Very similar to epidemic typhus but milder (>1% mortality rate). Treatment: Doxycycline or chloramphenicol

Question 15

Etiology/ transmission/ reservoirs of scrub typhus

Answer 15

Etiology: Orientia tsutsugamushi. Common reservoirs: Chiggers (larval mites). The bacterium can be transmitted in mites from generation to generation by transovarian transmission. Transmission: Chigger bite

Question 16

Scrub typhus clinical and treatment

Answer 16

Similar to epidemic typhus, except that rash is often absent and eschar develops at site of the chigger bite. Short-lived immunity because of antigenic variation. 7% mortality rate if untreated. Treatment: doxycycline or chloramphenicol

Question 17

spotted fever etiology and transmission

Answer 17

Rickettsia rickettsii. Reservoir: widespread in wild mammals, birds, and ticks (transovarial passage).Transmission: tick bite. American dog tick in the East, Wood tick in the West, Lone Star tick in the South and Southeast

Question 18

Spotted fever clinical

Answer 18

2-6 days after tick bite. Similar to typhus except that rash starts at extremities (wrists and ankles) and moves to trunk. Macular petechial rash. ≈7% mortality rate if untreated, but responds to tetracycline

Question 19

Spotted fever prevention and treatment

Answer 19

No vaccine. Prompt tick removal. Treatment: Doxycycline (not in pregnant)

Question 20

What kinds of cells do Ehrlichia and anaplasma species infect

Answer 20

their host target cells are phagocytic cells and they multiply within phagosomes

Question 21

Clinical features of ehrlichiosis

Answer 21

fever, headache, and often, multisystem involvement. NO rash. leucopenia and thrombocytopenia

Question 22

List diseases caused by ehrlichieae

Answer 22

Human Monocytotrophic Ehrlichiosis and Human Anaplasmosis

Question 23

Etiology/ transmission/ reservoirs of human monocytotrophic ehrlichiosis

Answer 23

Ehrlichia chaffeensis, Ehrlichia ewingii. Common reservoir: deer. Transmission: bite from a hard tick (lone star tick, brown dog tick, american dog tick)

Question 24

human monocytotrophic ehrlichiosi clinical

Answer 24

Incude fever, headache, chills, malaise, muscle pain, nausea, vomiting, diarrhea, confusion, conjunctival injection (red eyes), rash (60% of children, less than 30% of adults) erythroderma (sunburn-like rash) may occur in some patients. Some patients present with a rash very similar to RMSF. Thrombocytopenia, leukopenia or elevated LFTs

Question 25

human monocytotrophic ehrlichiosis pathogenesis

Answer 25

Infect monocytes and macrophages. Can be fatal in immunocompromised individuals. Disease caused by E. ewingii is usually less severe

Question 26

human monocytotrophic ehrlichiosis diagnosis

Answer 26

rapid: PCR from whole blood. During first week blood smear shows morulae (microcolonies of ehrlichiae) in the cytoplasm of white blood cells. Serology; immunofluorescence using antigen to detect antibodies. IgG is usually low/ negative in first week, and elevated by 2-4 weeks later.

Question 27

human monocytotrophic ehrlichiosis treatment

Answer 27

Tetracycline or doxycycline

Question 28

Human Anaplasmosis etiology, transmission, reservoir

Answer 28

Anaplasma phagocytophila. Common reservoir: deer. Transmission: bite from the same Ixodes tick as Lyme disease (soft tick)

Question 29

Human Anaplasmosis pathogenesis

Answer 29

Infect circulating neutrophils

Question 30

human anaplasmosis diagnosis and treatment

Answer 30

diagnosis: Inclusion bodies in neutrophils. Serology (IFA) (Note: some patients develop antibodies that cross-react in tests for Lyme disease). Treatment: doxycycline

Question 31

name the bacteria body louse can carry

Answer 31

rickettsia (prowazekii) causes epidemic typhus, Bartonella quintana causes trench fever, Borrelia quintana causes bacillary angiomatosis peliosis.

Question 32

Name flea assocated bacteria

Answer 32

Bartonlla henelae causes cat scratch fever. Rickettsia typhi causes endemic typhus