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Rickettsiae

Collage of Medicine

Dep. Of Microbiology

Assist. Proph Dr. Ilham alsaedi

Rickettsiae

     The human pathogens in the family(Rickttsiaceae), are small bacteria of the genera Rickettsia, Orientia, Coxiella and Erlichia.

Important properties:

1-       Rickttsiae are pleomorphic coccobacilli, appearing either as short rods.

2-       They do not stain well with Gram´s stain but are readily visible under the light  microscope when stained with Gimsa stain.

3-       Grow in the yolk sac of the embyonated egg and cell culture, but not bacteriologic media.

4-       Rickttsiae are obligate intercellular bacteria, because they are unable to produce sufficient energy to replicate extracellularly, they require Coenzyme A,NAD and energy from host cell. Therefore, Rickettsia must be grown in cell culture.

5-       Rickttsiae have Gram-negative cell wall structures that include peptidoglycan-containing muramic acid and di-aminopemalic acid.

6-       Rickttsiae grow in different part of the cell

a-       Typhus group, R. prowazekii in cytoplasm.

b-       Spotted fever group, R. rickettsii in nucleus.

c-       Coxiellae ,C.burnetti in cytoplasm vacuoles.

7-       Rickttsial growth is enhanced in the presence of sulfonamides and the disease are made more sever by the drugs, but para-amino benzoic acid (PABA),tetracycline and chloramphenicol are effective and may be suggested for treatment.

8-       Rickttsiae are quickly destroyed by heat, drying, and bacteriocidal chemicals, except Q-fever organism (R. burnettii) resistant to drying and survive pasteurization at 60°C for 30 min. and can survive for months in dried feces or milk. This may be due to the formation of endospore like structure.

Virulence factors:-

1-Rickttsia arephagocytosed into eukaryotic cells then break down the phagosome membrane by phospholipase A.

2-There is no evidence of toxin produced or immune complex formation as virulence factors.

Transmission and Epidemiology:

*All rickttsial disease are zoonoses (i.e., they have animal reservoir such as cattle, sheep, dogs, rodents) except epidemic typhus which occurs only in human because causative organism, R. prowazekii is transmitted from Peron to person by human body louse.

*Rout of infection:

   Human infection is acquired by inhaling the dust contaminated     by Rickttsiae, derived from animals and their products. Infection may occur by ingestion of infected milk. Also the Rickttsiae are transmitted to human by the bite of arthropod(ticks, mites, lice, and fleas which serve as vectors and reservoir).

*Q-Fever:

       Is recognized around the world and occur mainly in person associated with goats, sheep, dairy cattle.

Spotted fever occur in South and North America, Africa, Australia. Typhus disease is world wide infection occur in Balkan ,Asia ,Africa, Mexico and  the Andes mountains of South America.

Pathology:

Rickettsiae, except C. burnetii, multiply in endothelial cells of small blood vessels and produce vacuities.

The cell become swollen and necrotic, and there is thrombosis of the vessel, leading to rapture and necrosis.

In the brain, aggregation of lymphocytes, leukocytes and macrophages are associated with the blood vessel of the gray matter, these are called typhus nodules. The heart shows similar lesions of the small blood vessel. Other  organs may also be involved.

Disease caused by Rickettsia:

A-Spotted fever:

Is caused by R. rickettsii, R. australis, R. conorii, R. sibirica.

The bacteria invade vascular epithelial cells and become widely disseminated. After 2-6 days from tick bite, the typical clinical feature is rash that appears on(hands, feet and spread on trunk) and non-specific symptoms e.g. fever, sever headache, myalgia, mental confusion and coma.DIC thrombosis and blockage of small blood vessels may be occur in severe cases.

B-Typhus fever:

Cause by R. prowazekii. Recurrent from of epidemic is called(Brill-Zinsser disease).The R. prowazekii can persist for many years in the lymph nodes without any symptoms. The disease occurs in local population of typhus areas to place where the disease does not exist.

It can be distinguished from primary infection by early arising of IgG antibodies rather than IgM detected after primary infection. Weil-Felix reaction is negative.

C-Q(query)fever:

    Caused by C. burnetii, the infection characterized by fever, headache, prostration, skin rash and enlargement of spleen and liver. This disease like influenza or nonbacterial pneumonia. There is no rash or local lesions. rarely infective endocarditis develops. The Weil-Felix test is negative but there is arise in titer of specific antibodies.

Lab. Diagnosis:

* Isolation of Rickettsia is difficult and of limited usefulness in diagnosis.

* Serologically by using ELISA, CFT, Immunofluresnce, Weil-Felix reaction.

Control:

1-       By reduction exposure to arthropod by wearing protective clothing and using insecticide or by elimination of rodents.

2-       Drug of choice for all reckettsial disease is tetracycline, with chloramphenicol as a second choice.