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Corynebacterium diphtheriae (Diphtheria)
• Morphology and culturing. Diphtheria are Gram-positive rods.
Cells tend to group in V or Y arrangements.
• Facultative anaerobes. Loffler nutrient medium, which consists
of coagulated serum and nutrient broth, is still used for the
primary cultures. Selective indicator mediums containing
tellurite are used in selective culturing. K tellurite is used to
inhibit the accompanying flora.
Diphtheria
• Extracellular toxin. Diphtheria toxin consists of
two functionally distinct fragments, A and B,
whereby B stands for binding to receptors of
target cells and A stands for toxic activity.
Fragment A irreversibly blocks protein synthesis
translation in the target cells, which then die.
• Pathogenesis and Clinical Picture
Local infection. Infection of the mucosa of tonsils, pharynx,
nose, and conjunctiva.. The pathogens invade the host
through these portals, reproduce, and produce toxin,
resulting in local cell damage. The inflammatory reaction
leads to collection of a grayish-white exudate “diphtherial
pseudomembrane” consisting of fibrin, dead granulocytes,
and necrotic epithelial cells. This coating adheres quite
strongly to the mucosa. It may extend into the larynx,
affecting respiration. Regional lymph nodes are highly
swollen.
a Hemorrhaging
of the nasal mucosa
(endothelial damage). Pronounced
cervical adenopathy
and swelling, creating
a bull neck appearance.
Thick coating (membrane)
on highly swollen
tonsils (so-called diphtherial
pseudomembrane), causing
respiratory stridor.
• Diagnosis. The method of choice is detection and
identification of the pathogen in cultures from local infection
foci. The specimen is plated out on Loffler medium and a
selective indicator medium. Identification is based on both
morphological and physiological characteristics.
The toxin is detected by the Elek's immunodiffusion test. A
molecular method is now also being used to identify the
toxin gene. Toxin detection is necessary for a laboratory
diagnosis of diphtheria because of the occurrence of toxin-
negative strains.
• Therapy. Antitoxic serum therapy is the
primary treatment and it must commence as
soon as possible if diphtheria is suspected.
This treatment is supplemented by
administration of penicillin or erythromycin.
• Epidemiology and prevention. Humans are the sole
pathogen reservoir for diphtheria. Infection sources
include infected persons and carriers (rare). The
disease is usually transmitted by droplet infection. The
incubation period is two to five days.
• Protective immunization with diphtheria toxoid is the
most important preventive measure. Exposure
prophylaxis involves isolation of infected persons until
two cultures from specimens taken at least24 hours
apart are negative.
Listeria
• Listeria monocytogenesare is the only human pathogen.
• Morphology and culturing:
They are small Gram-positive rods with peritrichous flagella.
They show greater motility at 20°C than at 37°C.
• Culturing is successful under aerobic conditions on blood agar.
Following incubation for 18 hours, small gray colonies surrounded by
hemolytic zones appear. The zones are caused by listeriolysin O.
• Listeriae can also reproduce at 5–10ºC, which fact can be used in their
selective enrichment (“cold enrichment”).
• Pathogenesis.
– Adherence. To phagocytic cells (e.g., macrophages) and non-
phagocytic cells (e.g., enterocytes).
• Invasion: Endocytosis, induced by the protein internalin
on the surface of the listeriae. Formation of the
endosome.
• Destruction of the endosome: The virulence factor
listeriolysin forms pores in the endosomal membrane,
releasing the listeriae into the cytoplasm. & Replication of
the listeriae in the cytoplasm of infected cells.
• Clinical characteristics:
Listeriae are classic opportunists. The course of most infections
is clinically silent.
Symptoms resembling a mild flu do not occur in
immunocompetent persons until large numbers of pathogens
(large number 10 10) enter the gastrointestinal tract with food.
Massive infections frequently cause symptoms of
gastroenteritis.
Listeriosis can take on the form of sepsis and/or
meningoencephalitis in persons with T cell defects or
malignancies, in alcoholics, during cortisone therapy, during
pregnancy, in elderly persons and in infants.
• Diagnosis:
Requires pathogen identification by means of
microscopy and culturing.
• Therapy:
Amoxicillin, penicillin G, or cotrimoxazole.

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Diphtheria and llisteria - 3.pptx

  • 1. Corynebacterium diphtheriae (Diphtheria) • Morphology and culturing. Diphtheria are Gram-positive rods. Cells tend to group in V or Y arrangements. • Facultative anaerobes. Loffler nutrient medium, which consists of coagulated serum and nutrient broth, is still used for the primary cultures. Selective indicator mediums containing tellurite are used in selective culturing. K tellurite is used to inhibit the accompanying flora.
  • 3. • Extracellular toxin. Diphtheria toxin consists of two functionally distinct fragments, A and B, whereby B stands for binding to receptors of target cells and A stands for toxic activity. Fragment A irreversibly blocks protein synthesis translation in the target cells, which then die.
  • 4. • Pathogenesis and Clinical Picture Local infection. Infection of the mucosa of tonsils, pharynx, nose, and conjunctiva.. The pathogens invade the host through these portals, reproduce, and produce toxin, resulting in local cell damage. The inflammatory reaction leads to collection of a grayish-white exudate “diphtherial pseudomembrane” consisting of fibrin, dead granulocytes, and necrotic epithelial cells. This coating adheres quite strongly to the mucosa. It may extend into the larynx, affecting respiration. Regional lymph nodes are highly swollen.
  • 5. a Hemorrhaging of the nasal mucosa (endothelial damage). Pronounced cervical adenopathy and swelling, creating a bull neck appearance.
  • 6. Thick coating (membrane) on highly swollen tonsils (so-called diphtherial pseudomembrane), causing respiratory stridor.
  • 7. • Diagnosis. The method of choice is detection and identification of the pathogen in cultures from local infection foci. The specimen is plated out on Loffler medium and a selective indicator medium. Identification is based on both morphological and physiological characteristics. The toxin is detected by the Elek's immunodiffusion test. A molecular method is now also being used to identify the toxin gene. Toxin detection is necessary for a laboratory diagnosis of diphtheria because of the occurrence of toxin- negative strains.
  • 8. • Therapy. Antitoxic serum therapy is the primary treatment and it must commence as soon as possible if diphtheria is suspected. This treatment is supplemented by administration of penicillin or erythromycin.
  • 9. • Epidemiology and prevention. Humans are the sole pathogen reservoir for diphtheria. Infection sources include infected persons and carriers (rare). The disease is usually transmitted by droplet infection. The incubation period is two to five days. • Protective immunization with diphtheria toxoid is the most important preventive measure. Exposure prophylaxis involves isolation of infected persons until two cultures from specimens taken at least24 hours apart are negative.
  • 10. Listeria • Listeria monocytogenesare is the only human pathogen. • Morphology and culturing: They are small Gram-positive rods with peritrichous flagella. They show greater motility at 20°C than at 37°C. • Culturing is successful under aerobic conditions on blood agar. Following incubation for 18 hours, small gray colonies surrounded by hemolytic zones appear. The zones are caused by listeriolysin O. • Listeriae can also reproduce at 5–10ºC, which fact can be used in their selective enrichment (“cold enrichment”).
  • 11. • Pathogenesis. – Adherence. To phagocytic cells (e.g., macrophages) and non- phagocytic cells (e.g., enterocytes). • Invasion: Endocytosis, induced by the protein internalin on the surface of the listeriae. Formation of the endosome. • Destruction of the endosome: The virulence factor listeriolysin forms pores in the endosomal membrane, releasing the listeriae into the cytoplasm. & Replication of the listeriae in the cytoplasm of infected cells.
  • 12. • Clinical characteristics: Listeriae are classic opportunists. The course of most infections is clinically silent. Symptoms resembling a mild flu do not occur in immunocompetent persons until large numbers of pathogens (large number 10 10) enter the gastrointestinal tract with food. Massive infections frequently cause symptoms of gastroenteritis. Listeriosis can take on the form of sepsis and/or meningoencephalitis in persons with T cell defects or malignancies, in alcoholics, during cortisone therapy, during pregnancy, in elderly persons and in infants.
  • 13. • Diagnosis: Requires pathogen identification by means of microscopy and culturing. • Therapy: Amoxicillin, penicillin G, or cotrimoxazole.