Gram positive rod shaped, causes acne.It is most often the result of male sex hormones that stimulates sebaceous glands to increase insize and secrete more sebum. It occurs in both sexes, because the hormones are produced by the adrenal glands as well as by the testes. Microorganisms feed on sebum, and ducts of the glands and  surrounding tissues become inflamed.

            ‘Black heads’ are a mild form of acne in which hair foliicles and sebaceous glands become plugged with sebum and keratin. In most severe cases, the plugged ducts becomes inflammed, ruptured and releases secretions. Propionibacterium acnes infect the area and cause more inflammation, more tissue destruction. Such lesions can be widely distributed over the body, and some becomes encysted in connective tissue.

            Acne is treated with frequent cleansing of the skin and topical ointments to reduce the risk of infection. Oral antibiotics such as tetracycline prescribed in low doses to control bacterial infections. The drug Accutane, derived from a molecule related to Vitamin A, is now used to treat severe, persistent acne. It causes side effects such as intestinal bleeding. In most cases acne disappears or decreases in severity as the body adjusts to the hormonal changes of puberty and as the functioning of sebaceous glands stabilizes.

                                      PHYLUM: BACTEROIDETES

        3 classes: Bacteroides, Flavobacteria, Sphingobacteria
       Bacteroides contains anaerobic, gram –ve ,non sporing motile or nonmotile rods of various shapes.These are chemoheterotrophic & usually produce a mixture of organic acids as fermentation end products.These bacteria grow in habitats such as the oral cavity & intestinal tract of humans & other animals & the rumen of ruminants.
Often they benefit their host.The species in ruminants Bacteroides ruminicola ferments starch, pectin, & other COH. The Bacteroides in humans provides extra nutrition by degrading cellulose, pectins & other complex COHs.
The members are also involved in human disease. They are associated with diseases of major organ systems ie. From CNS to the skeletal system. Bacteroides fragilis is an anaerobic pathogen found in abdominal, pelvic, pulmonary and blood infections.


              - caused by B.fragilis & other Enterobacteriaceae members.They cause septic shock,accompanied by low BP and the collapse of blood vessels.Antibiotics
 worsen the situation as when they kill micro organisms,the disintegrating 
 organisms release large quantities of hemolysin,causing more damage to host’s              
 blood vessel,and blood pressure drops further.
                 Symptoms are fever,shock,red streaks due to inflamed lymphatic vessels, 
beneath the skin.
      Diagnosis by blood culturing, urine culture etc.
            Bacteroides have a typical G-ve cell wall structure.surrounded by a     polysaccharide capsule. The LPS of cell wall has little or no endotoxin activity.This is because  lipid A of LPS lacks phosphate groups on the glucosamine residues and number of fatty acids linked to the amino sugars in reduced.

   Virulence factors

         A variety of virulence factors that facilitate adherence of the organisms to host tissues, protection from the host immune response & tissue destruction.
  Adhesins- Capsule, fimbriae  are present.
  Resist O2 Toxicity- because of  superoxide dismutase & catalase.
  Antiphagocytic-  Capsule, LPC, Volatile fatty acids.
Tissue  destruction- Hemolysins, Proteases, Collagenase, Fibrinolysin, Neuraminidase, NAGase etc.
Skin & soft tissue infections:
           Although anaerobic G-ve bacteria are not part of the normal flora of the skin, they can be introduced by a bite or by contamination of infected surface. In  some cases the organisms may simply colonize a wound but not produce disease, while sometimes colonization quickly progress to life-threatening disease such as myonecrosis. B.fragilis  is the organism mostly associated.


Intraabdominal infections- B.fragilis  is responisible for abscess formation in gynecological infections.
  Laboratory diagnosis:
1) Microscopy- Suspected samples collected & observed under microscope after staining.
2) Culture- Specimens should be collected & transported to the laboratory in an oxygen free system, promptly inoculated on anaerobic media & cultured anaerobically. Since most anaerobe infections are endogenous, it is important that the specimens collected should not contaminated with normal flora on the adjacent mucosal surface.
The preliminary indentification is made by Gram stain & colony morphology, resistance to kaesamycin , vancomycin, stimulated growth in 20% bile.
    Prevention & Control :
               B.fragilis   produce beta-lactamase, therefore are resistant to penicillin & cephalosporins.High concentrations of some penicillins, beta-lactamase inhibitors can be used. Metronidazole is active, & is the choice for treatment.
      Since  it is an important part of the normal flora, the disease is virtually impossible to control. It is important to recognize that diagnostic or surgical procedures disrupting the natural barriers around the mucosal surfaces can introduce these organisms into sterile sites. If these barriers are invaded, tretment with antibiotics may be indicated.


                 -are small, G-ve  bacilli adapted to obligate intercellular parasitism, transmitted by arthropod vectors. They are primary parasites of arthropods such as lice, ticks, in which they are found in the alimentary canal. In vertebrates, they infect vascular endothelium, recticuloendothelial cells.
        This pleomorphic coccobacilli are nonmotile, non capsulated. They stain bluish purple with Giemsa. It has a 3 layered cell wall, a trilaminar plasma membrane, outer
Slime layer.
         Growth occurs in the cytoplasm of infected cells, nucleus etc. The optimium
temperature  is 32- 35 C. They are readily cultivated in the yolk sac of chick embryos,
HeLa cells etc, in  arthropods.
          They are  inactivated by physical, chemical agents. They are rapidly destroyed at room temperature. When separated from host components, susceptible to tetracycline, chloranphenicol, ciprofloxacin. Sulfonamides enhance the growth & worsen the condition of patients.
           Rickettsia have species & group specific antigens, such as surface protein antigens (SPA) & outer membrane proteins (OMP), also a third surface antigen ie. an
Alkali stable  polysaccharide. This antigen is found in some Rickettsiae & in some strains of Proteus bacilli.
Weil-Felix Reaction:
           During world war 1st Austrian Bacteriologists Edmond Weil & Arthur Felix were in charge of diagnosing typhus fever, an arthropod borne, caused by Rickettisis in the Austrian army. In 1916, they developed the agglutination test for typhus.
The Weil-Felix reaction is based on the detection of cross-reactive antibodies. In this test, antibodies produced in response to a particular rickettsial infection, agglutinate bacterial strains of Proteus   such as OX-19,OX-2,OX-k. These  cross reactions occurs because rickettsial strains possess cell wall antigen ie. alkali stable polysaccharide similar to the ‘O’ cell wall antigen of Proteus strains. But Proteus  sps. are normal flora of human beings & may cause urinary tract tract infections. Therefore the presence of antibodies to Proteus OX strain could not be considered an absolute criterion for the presence of rickettsial disease.


         Rickettsias are named after Howard T.Ricketts who identified them as the causative agents of Typhus & Rocky Mountain spotted fevers. [Died of lab infections from these highly infections microorganisms].
Typhus fever forms grow in the cytoplasm of infected cells. Rocky Mountain spotted fever grow in both nucleus & the cytoplasm. They are cultured only in cells, embryonated eggs. Despite improved laboratory designs & equipments, vaccine, the infection is common & fatal.
The organisms invade, damage the cells of blood vessel linings and cause the linings to leak, which causes skin lesions & petechiae-pin point hemorrhages common in skin folds. It also causes fever, headache, extreme weakness, liver & spleen enlargement, skin rashes.
1) Typhus fever – 3 types    a) Epidemic typhus
                                             b) Endemic typhus
                                             c) Scrub typhus.
Epidemic typhus – [Classic, European/ Louse borne typhus] caused by Rickettsia prowazekki. The disease is common during wars, over crowding, poor sanitation. The disease is transmitted by human  body louse, Pediculus humanis corporis. After a louse feeds on an infected person, rickettsias multiply in its digestive tract & are shed in its faeces. When a louse bites, it defecates & the infected lice deposit organism next to a bite & die of typhus in a few weeks. As victims scratch bites, they inoculate organisms into the wound. The infected lice abandon dead bodies or people with high fevers, moving to & infecting new hosts.
After 12 days incubation, fever & headache is abrupt & after 7 days  a rash on the trunk & spread to extremities, but spares face, palm & soles.
Antibiotic therapy should be started immediately. The disease can be prevented by eradicating lice with insecticides & maintaining hygienic living conditions. A vaccine is available. Recovery gives lifetime immunity, except in Brill-Zinser disease.
Brill-Zinser disease – is a recurrence of typhus infection, named after, Nathan Brill & Hans Zinser in 1930s. This disease has milder symptoms, shorter duration & no skin rash. It is caused by reactivation of latent organisms harbored in lymph nodes. Despite rigorous treatment, some victims of typhus still develop this disease. It can be distinguished from epidemic typhus by the type of antibodies formed . epidemic typhus first elicits IgM & then IgG antibodies, whereas Brill-Zinser disease elicity. IgG antibodies being a secondary response.
Endemic typhus- [Murine typhus- because of the association with rats, flea-borne typhus] caused by R.typhi. Rat flea Xenopsylla cheopis  multiplies in the gut of the flea & shed in its faeces. The fleas defecates while biting host, & host scratches the organisms enter into through the wound. After 10- 14 days incubation fever, chills, headache, followed by a rash in 3- 4 days. It lasts about 2 weeks if untreated.
Scrub typhus [tsutsugamoshi disease] caused by R.tsutsugamoshi transmitted by a bad little bug or mite, that feeds on rats in Japan, Australia. After 10-12 days incubation, scrub typhus begins with fever, chills, headache. Many patients develop sloughing lesions at the bite sites & later a spotty rash. Infectious prevented by controlling mite population.
Rocky Mountain spotted fever
            First recognized in Rocky Mountain states in 1900. The disease is caused by     R.rickettsii, transmitted by ticks of the genus, Dermacentor. Ticks are not harmed by  the rickettsiae & remain infected for life. The organisms are shed in ticks faeces but transmission to human beings primarily by a bite as the organism invade the salivary gland of the ticks. After 3-4 days incubation, onset of fever, headache, weakness is abrupts, followed in 2-4 days by a rash. The rash begins on ankles & wrists, prominent on palms & soles & progresses toward the trunk (just reverse of typhus fever). Spots are caused by blood leaking out of damaged blood vessels beneath the skin surface, they coalesce as blood leaks from many damaged sites. Blood vessels in the organs throughout
the body are damaged.
The fever can be prevented by wearing protective clotting & by vigilantly inspecting clothing & skin during visits to tick infected areas. Inspecting children’s hair is important. Eventhough vaccine is available, it is not effective  completely.
Laboratory diagnosis
         Rickettsial diseases may be diagnosed in the laboratory either by isolation of the rickettsiae or by serology. They can be isolated in male guinea pigs or mice from inoculated intraperitoneally. The animals are observed for 3-4 weeks & the temperature is recorded daily. Their response varies with Rickettsial species. Some may dies. Smears from peritoneum, spleen of infected animals may be stained with Giemsa.
Serological diagnosis can be done by Weil-Felix reaction (explain). The test is usually done as a tube agglutination or rapid slide agglutination.
The most frequently used serological method using rickettsial antigens is the complement fixation test. This may be done using the group-specific soluble antigen, or the type-specific rickettsial antigen.
          Coxiella burnetti is pleomorphic rods, spheres. It is filterable. In dried faeces, wool it survives for a year at 4 C. It is not inactivated by 60C, 1% phenol. In milk it survive holding method pasteurization, while susceptible to flash method. It grows well in the chick embryo yolk sac. It has 2 forms –large & small variants. The large-cell variant produces terminal endospore, thereby giving resistance.
           C.burnetti causes Q-fever (first discovered in Queensland, Australia, Q-stands for query- because determining which organism caused it remained a question for a long time). Unlike other rickettsias, this organism survives long periods outside cells & can be transmitted aerially or by ticks.
Once C.burnetti cells with endospore like bodies inside them have been inhaled, they are phagocytized by host cells, and they grow in phagolysosomes of host cells. There they respondto the acidic conditions by increasing their metabolism & multiplying rapidly until they almost fill infected cells. Eventually  the cell ruptures releasing the pathogenic bacteria. These pathogens, when spread by the blood stream, infect other body cells.
           C.burnetti exist all over the world, especially in cattle, sheep-raising areas. Wild animals & cattle are normal hosts. The bacteria are transmitted via tick bites, faeces & genital secretions of infected animals. Humans become infected by inhaling aerosol droplets from infected domestic animals. Farmers become infected while attending a cow giving birth or miscarrying if the placenta is laden with organisms. Slaughter house and tannery workers become infected by inhaling dried tick faeces from animal hides.because of its resistance to drying, Coxiella remain viable in the environment for long periods of time. Transmission to human also occurs by the ingestion of milk from contaminated animals. Flash pasteurization eliminates the hazard.
            Chills, fever, headache,   malaise & severe sweats. The incubation period is 18-20 days. Diagnosis by serologic testing or by direct immunofluorescent antibody staining.
            Treatment with antibodies – tetracycline,  fluoroquinolone. Lifelong immunity follows, a vaccine is available.
            Untreated or inadequately treated Q fever, remits. Corisone treatment reactivate it. In chronic cases, endocarditis & heart value infections are seen.

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