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THE CAUSATIVE AGENTS OF
ANAEROBIC INFECTIONS
SAFINA HUSSEIN MEENA
GM 20-04
INTRODUCTION
Anaerobic bacteria are a group of bacteria that are characterized by their ability to
grow only in an atmosphere containing less than 20% oxygen; they range in
between those that can barely grow in 20% oxygen to those that can grow only in
less than 0.02%.
Groups of bacteria depending on
atmospheric oxygen
Obligate aerobes:
grow est in 20%
oxygen
Aerotolerant: ca grow
in oxygen to some
extent but prefer low
oxygen concentration
for rapid growth
Microaerophilic:
they require a
reduced oxygen
concentration
~5% to grow
optimally
Facultative aerobes:
can grow under both
circumstances of either
aerobic or anaerobic
WHY THEY ARE ANAEROBIC
➔ These type of bacteria are not able to survive in the presence of oxygen (or have
a reduced growth in normal/high concentrations of oxygen) due to the
production of superoxide radical in the presence of oxygen which is fatal for the
bacteria alongside other organisms.
➔ They lack cytochrome so they cannot use oxygen as a hydrogen acceptor.
➔ Most Lack Catalase & Peroxidase.
➔ Contain flavoprotein so in the presence of air that has >10% oxygen they
produce H2O2 which is toxic
CLASSIFICATION OF MEDICALLY IMPORTANT
ANAEROBES
EPIDEMIOLOGY
Anaerobes are part of the normal flora of the human body particularly the oral
cavity, human bowel and female genital tract. Infections from anaerobes can occur
due to a breakdown in the mucocutaneous barrier or immunosuppression.
Almost all infections are indigenous except:
● Tetanus
● Infant, wound botulism
● Gas gangrene (some cases)
● Bites
● C .difficile (nosocomial)
PATHOGENESIS OF ANAEROBIC INFECTIONS
The virulence factors which assist anaerobic
infections include:
- Adhesion factors: fimbriae and lectin
- Invasion factors: phospholipase C, LPS and
proteases
- Capsular resistance to phagocytosis
- Factors involved in tissues destruction such as:
fibrinolysis, acetylglucosaminidase and collagen
production
FEATURES OF ANAEROBIC INFECTIONS
Infections are always near to the site of the body which are habitat.
1. Infection from animal bites.
2. Deep abscesses.
3. The infections are also polymicrobial.
4. Gas formation, foul smell.
5. Detection of "Sulphur granules"' due to actinomycosis.
6. Failure to grow organism from pus if not culture anaerobically.
7. Failure to respond to usual antibiotics.
DIAGNOSIS OF ANAEROBIC INFECTIONS
A laboratory diagnosis for anaerobes is only done when the infection is suspected to be anaerobic due
to certain clues such as a foul-smelling discharge, gas, necrotic tissue, abscess formation, the unique
morphology of certain anaerobes on Gram's Stain, and failure to obtain growth on aerobic culture
despite the presence of organisms on Gram-stain direct smear.
when an anaerobic infection is suspected;
➔ Specimens have to be collected from the site containing necrotic tissue.
➔ Pus is better than swabs.
➔ Specimens have to be sent to the laboratory within 1/2 hour why? otherwise the bacteria dies.
➔ Fluid media like cooked meat broth are the best culture media because they provide nutrition in
an anaerobic environment.
➔ Specimens are preferably extracted from abscesses or deep wounds and incubated anaerobically
(in nitrogen) for 48 hours.
PREVENTION AND TREATMENT
FOR PREVENTION:
You can help prevent anaerobic infections on your skin and soft tissues by taking
proper care of cuts as soon as they occur as most anaerobic infections are
opportunistic infection of the indigenous flora.
FOR TREATMENT:
Metronidazole has broad use in anaerobic infections; other anaerobic antibiotics
include: clindamycin, penicillin beta lactamase inhibitor combination, second
generation cephalosporins, carbapenems and quinolones,
RICKETTSIAE
These are obligate intracellular parasites that are transmitted to humans by
arthropods which serve as both vector and reservoir. The typical clinical
manifestations of rickettsiae infections are fevers, rashes and vasculitis.
MORPHOLOGY:
➔ They are pleomorphic coccobacilli appearing either as short rods or cocci. They
do not stain well with gram stain but are easily visible under the light
microscope when stained with Giemsa stain.
➔ They grow readily in yolk sacs of embryonated eggs
➔ They have a gram negative cell wall structure that consists of peptidoglycan
containing muramic acid and diaminopimelic acid.
PATHOGENESIS
Rickettsiae multiply in endothelial cells of small blood vessels and produce
inflammation of blood vessels, i.e. vasculitis characterized by lymphocytes that
surround the blood vessels. The cells become swollen and necrotic; there is
thrombosis of the vessel leading to vessel rupture and necrosis.
Vascular lesions are prominent in the skin and disseminated intravascular
coagulation and vascular occlusion may develop. In the brain, aggregations of
lymphocytes, polymorphonuclear leukocytes and macrophages are associated with
the blood vessels of the gray matter referred to as typhus nodules.
CLINICAL FINDINGS
Rickettsial infections are characterized by fever, headache, ,malaise, prostration,
skin rash and enlargement of the spleen and liver.
RICKETTSIAL INFECTIONS
TYPHUS
GROUP
SPOTTED
FEVER
GROUP
TRADITIONAL
GROUP
SCRUB
TYPHUS
GROUP
LABORATORY DIAGNOSIS
Isolation of rickettsiae is technically difficult and has limited usefulness. They are
recovered most frequently from blood drawn soon after onset of illness.
Real time PCR methods have enhanced sensitivity and allow diagnosis before the
occurrence of a serological response.
PREVENTION AND TREATMENT
FOR PREVENTION:
Wear long sleeved protective clothing and a broad brimmed hat to reduce the risk of infection when
undertaking activities where human contact with ticks, lice, mites or fleas may occur, such as
bushwalking and camping in infected areas.
FOR TREATMENT:
● Tetracyclines especially doxycycline are effective medications as long as the treatment is started
early.
● Chloramphenicol also can be effective. Sulfonamides enhance the disease and are usually
contraindicated
These antibiotics are only able to suppress the growth of the rickettsiae; total recovery depends on
the immune system of the patient.
BORRELIA
The genus Borrelia cause two important human diseases: Lyme disease and
relapsing fever.
IMPORTANT SPECIES
OF BORRELIA
B. burgdorferi:
causes Lyme
disease
B. recurrentis: causes
relapsing fever which
is louse-borne
B. spp: causes relapsing
fever endemic that is tick-
borne.
MORPHOLOGY
● Are spirochete bacteria that are neither gram negative or gram positive due to
their property of staining poorly with Gram stain.
● They stain well with aniline dyes, e.g. Giemsa or Wright stain
● Can be easily seen by light microscopy when present in smears of peripheral
blood from patients with relapsing fever but not those Lyme disease.
● Are microaerophilic and have complex nutritional needs
● Culture media is generally unsuccessful
PATHOGENESIS AND IMMUNITY
The growth of borrelia is regulated by differential gene expression with up and down regulation of
outer surface proteins.
The incubation period is 3–10 days. The onset is sudden, with chills and an abrupt rise of
temperature. During this time, spirochetes abound in the blood. The fever persists for 3–5 days and
then declines, leaving the patient weak but not ill.
The afebrile period lasts 4–10 days and is followed by a second attack of chills, fever, intense
headache, and malaise. There are 3–10 such recurrences, generally of diminishing severity.
During the febrile stages (especially when the temperature is rising), organisms are present in the
blood; during the afebrile periods, they are absent.Antibodies against the spirochetes appear during
the febrile stage, and the attack is probably terminated by their agglutinating and lytic effects
CLINICAL DISEASES
LABORATORY DIAGNOSTICS
Because culture is generally unsuccessful, diagnosis of diseases caused by borreliae
is by serology (for Lyme disease) or microscopy (for relapsing fever)
TREATMENT AND PREVENTION
FOR TREATMENT:
Tetracyclines, erythromycin, and penicillin are all believed to be effective. Treatment
for a single day may be sufficient to terminate an individual attack.
FOR PREVENTION:
Prevention is based on avoidance of exposure to ticks and lice and on delousing
(cleanliness, insecticides)
 Anaerobic infections,Bocelli and ricketssia

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Anaerobic infections,Bocelli and ricketssia

  • 1. THE CAUSATIVE AGENTS OF ANAEROBIC INFECTIONS SAFINA HUSSEIN MEENA GM 20-04
  • 2. INTRODUCTION Anaerobic bacteria are a group of bacteria that are characterized by their ability to grow only in an atmosphere containing less than 20% oxygen; they range in between those that can barely grow in 20% oxygen to those that can grow only in less than 0.02%. Groups of bacteria depending on atmospheric oxygen Obligate aerobes: grow est in 20% oxygen Aerotolerant: ca grow in oxygen to some extent but prefer low oxygen concentration for rapid growth Microaerophilic: they require a reduced oxygen concentration ~5% to grow optimally Facultative aerobes: can grow under both circumstances of either aerobic or anaerobic
  • 3. WHY THEY ARE ANAEROBIC ➔ These type of bacteria are not able to survive in the presence of oxygen (or have a reduced growth in normal/high concentrations of oxygen) due to the production of superoxide radical in the presence of oxygen which is fatal for the bacteria alongside other organisms. ➔ They lack cytochrome so they cannot use oxygen as a hydrogen acceptor. ➔ Most Lack Catalase & Peroxidase. ➔ Contain flavoprotein so in the presence of air that has >10% oxygen they produce H2O2 which is toxic
  • 4. CLASSIFICATION OF MEDICALLY IMPORTANT ANAEROBES
  • 5. EPIDEMIOLOGY Anaerobes are part of the normal flora of the human body particularly the oral cavity, human bowel and female genital tract. Infections from anaerobes can occur due to a breakdown in the mucocutaneous barrier or immunosuppression. Almost all infections are indigenous except: ● Tetanus ● Infant, wound botulism ● Gas gangrene (some cases) ● Bites ● C .difficile (nosocomial)
  • 6. PATHOGENESIS OF ANAEROBIC INFECTIONS The virulence factors which assist anaerobic infections include: - Adhesion factors: fimbriae and lectin - Invasion factors: phospholipase C, LPS and proteases - Capsular resistance to phagocytosis - Factors involved in tissues destruction such as: fibrinolysis, acetylglucosaminidase and collagen production
  • 7. FEATURES OF ANAEROBIC INFECTIONS Infections are always near to the site of the body which are habitat. 1. Infection from animal bites. 2. Deep abscesses. 3. The infections are also polymicrobial. 4. Gas formation, foul smell. 5. Detection of "Sulphur granules"' due to actinomycosis. 6. Failure to grow organism from pus if not culture anaerobically. 7. Failure to respond to usual antibiotics.
  • 8. DIAGNOSIS OF ANAEROBIC INFECTIONS A laboratory diagnosis for anaerobes is only done when the infection is suspected to be anaerobic due to certain clues such as a foul-smelling discharge, gas, necrotic tissue, abscess formation, the unique morphology of certain anaerobes on Gram's Stain, and failure to obtain growth on aerobic culture despite the presence of organisms on Gram-stain direct smear. when an anaerobic infection is suspected; ➔ Specimens have to be collected from the site containing necrotic tissue. ➔ Pus is better than swabs. ➔ Specimens have to be sent to the laboratory within 1/2 hour why? otherwise the bacteria dies. ➔ Fluid media like cooked meat broth are the best culture media because they provide nutrition in an anaerobic environment. ➔ Specimens are preferably extracted from abscesses or deep wounds and incubated anaerobically (in nitrogen) for 48 hours.
  • 9. PREVENTION AND TREATMENT FOR PREVENTION: You can help prevent anaerobic infections on your skin and soft tissues by taking proper care of cuts as soon as they occur as most anaerobic infections are opportunistic infection of the indigenous flora. FOR TREATMENT: Metronidazole has broad use in anaerobic infections; other anaerobic antibiotics include: clindamycin, penicillin beta lactamase inhibitor combination, second generation cephalosporins, carbapenems and quinolones,
  • 10. RICKETTSIAE These are obligate intracellular parasites that are transmitted to humans by arthropods which serve as both vector and reservoir. The typical clinical manifestations of rickettsiae infections are fevers, rashes and vasculitis. MORPHOLOGY: ➔ They are pleomorphic coccobacilli appearing either as short rods or cocci. They do not stain well with gram stain but are easily visible under the light microscope when stained with Giemsa stain. ➔ They grow readily in yolk sacs of embryonated eggs ➔ They have a gram negative cell wall structure that consists of peptidoglycan containing muramic acid and diaminopimelic acid.
  • 11. PATHOGENESIS Rickettsiae multiply in endothelial cells of small blood vessels and produce inflammation of blood vessels, i.e. vasculitis characterized by lymphocytes that surround the blood vessels. The cells become swollen and necrotic; there is thrombosis of the vessel leading to vessel rupture and necrosis. Vascular lesions are prominent in the skin and disseminated intravascular coagulation and vascular occlusion may develop. In the brain, aggregations of lymphocytes, polymorphonuclear leukocytes and macrophages are associated with the blood vessels of the gray matter referred to as typhus nodules.
  • 12. CLINICAL FINDINGS Rickettsial infections are characterized by fever, headache, ,malaise, prostration, skin rash and enlargement of the spleen and liver. RICKETTSIAL INFECTIONS TYPHUS GROUP SPOTTED FEVER GROUP TRADITIONAL GROUP SCRUB TYPHUS GROUP
  • 13. LABORATORY DIAGNOSIS Isolation of rickettsiae is technically difficult and has limited usefulness. They are recovered most frequently from blood drawn soon after onset of illness. Real time PCR methods have enhanced sensitivity and allow diagnosis before the occurrence of a serological response.
  • 14. PREVENTION AND TREATMENT FOR PREVENTION: Wear long sleeved protective clothing and a broad brimmed hat to reduce the risk of infection when undertaking activities where human contact with ticks, lice, mites or fleas may occur, such as bushwalking and camping in infected areas. FOR TREATMENT: ● Tetracyclines especially doxycycline are effective medications as long as the treatment is started early. ● Chloramphenicol also can be effective. Sulfonamides enhance the disease and are usually contraindicated These antibiotics are only able to suppress the growth of the rickettsiae; total recovery depends on the immune system of the patient.
  • 15. BORRELIA The genus Borrelia cause two important human diseases: Lyme disease and relapsing fever. IMPORTANT SPECIES OF BORRELIA B. burgdorferi: causes Lyme disease B. recurrentis: causes relapsing fever which is louse-borne B. spp: causes relapsing fever endemic that is tick- borne.
  • 16. MORPHOLOGY ● Are spirochete bacteria that are neither gram negative or gram positive due to their property of staining poorly with Gram stain. ● They stain well with aniline dyes, e.g. Giemsa or Wright stain ● Can be easily seen by light microscopy when present in smears of peripheral blood from patients with relapsing fever but not those Lyme disease. ● Are microaerophilic and have complex nutritional needs ● Culture media is generally unsuccessful
  • 17. PATHOGENESIS AND IMMUNITY The growth of borrelia is regulated by differential gene expression with up and down regulation of outer surface proteins. The incubation period is 3–10 days. The onset is sudden, with chills and an abrupt rise of temperature. During this time, spirochetes abound in the blood. The fever persists for 3–5 days and then declines, leaving the patient weak but not ill. The afebrile period lasts 4–10 days and is followed by a second attack of chills, fever, intense headache, and malaise. There are 3–10 such recurrences, generally of diminishing severity. During the febrile stages (especially when the temperature is rising), organisms are present in the blood; during the afebrile periods, they are absent.Antibodies against the spirochetes appear during the febrile stage, and the attack is probably terminated by their agglutinating and lytic effects
  • 19. LABORATORY DIAGNOSTICS Because culture is generally unsuccessful, diagnosis of diseases caused by borreliae is by serology (for Lyme disease) or microscopy (for relapsing fever)
  • 20. TREATMENT AND PREVENTION FOR TREATMENT: Tetracyclines, erythromycin, and penicillin are all believed to be effective. Treatment for a single day may be sufficient to terminate an individual attack. FOR PREVENTION: Prevention is based on avoidance of exposure to ticks and lice and on delousing (cleanliness, insecticides)