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Since diphtheria results primarily from toxin absorption rather than microbial invasion, its control can be accomplished most effectively by immunization with toxoid. Toxoid, prepared by formalin treatment of diphtheria toxin, causes the body to produce antibodies that specifically neutralize the diphtheria toxin. The well-known childhood vaccination DPT consists of diphtheria and tetanus toxoids and pertussis vaccine, all three generally given together. Unfortunately, these immunizations have often been neglected, particularly among socioeconomically disadvantaged groups, and serious epidemics of the diseases have occurred periodically. Since the 1980s, there has been an active campaign in most of the United States to ensure that children who are entering school are immunized against diphtheria. As a result, today only a few cases of diphtheria are reported annually in the United States, as compared with 30,000 cases reported in 1936. Of concern is the finding that widespread childhood

Toxin precursor (inactive) -

A chain

B chain

Toxin precursor (inactive) -

A chain

B chain

Binding site

B chain attaches to receptor

Resistant cell membrane

Disulfide bond

Disulfide bond

Binding site

Cell membrane (susceptible cell)

B chain attaches to

receptor

Resistant cell membrane

Endocytosis begins

Cell membrane (susceptible cell)

Endocytosis begins

Acidification of vacuole

■ ADP • ribose-EF-2 + nicotinamide (inactivated)

Acidification of vacuole

■ ADP • ribose-EF-2 + nicotinamide (inactivated)

Figure 23.6 Mode of Action of Diphtheria Toxin The toxin precursor released from the bacterium is cleaved extracellularly into A and B chains joined only by a disulfide bond; the B chain attaches to a specific receptor on the cell membrane of a susceptible cell.The toxin enters the cell by endocytosis.With acidification of the endocytic vacuole, the A chain separates from the B chain and then enters the cytoplasm as an active enzyme that inactivates EF-2 (elongation factor 2) by ADP ribosylation. Since EF-2 is required for moving the ribosome on mRNA, protein synthesis ceases and the cell dies.

Nester-Anderson-Roberts: I IV. Infectious Diseases I 23. Respiratory System I I © The McGraw-Hill

Microbiology, A Human Infections Companies, 2003

Perspective, Fourth Edition

Table 23.4 Diphtheria

23.3 Bacterial Infections of the Upper Respiratory System 571

© Corynebacterium diphtheriae enters by inhalation.

© Infection established in nasal cavity and/or throat

© Toxin released, membrane forms

@ Toxin causes paralysis, damages heart muscle, kidneys, nerves

© Membrane may come loose and obstruct breathing

© Exit from body by respiratory secretions

Symptoms

Incubation period Causative agent

Pathogenesis

Epidemiology

Prevention and treatment

Sore throat, fever, fatigue, and malaise; membrane forms on tonsils and throat or in nose; paralysis, heart and kidney failure

2 to 6 days

Corynebacterium diphtheriae, a toxin-producing, non-spore-forming Grampositive rod

Infection in upper respiratory tract; exotoxin released and absorbed by bloodstream; toxin kills cells by interfering with protein synthesis; effect is on cells that have receptors for the toxin—mainly heart, kidney, and nerve tissue

Inhalation of infectious droplets; direct contact with patient or carrier; indirect contact with contaminated articles

Immunization with diphtheria toxoid; given to children at 6 weeks, 4 months, 6 months, 18 months, and 4 to 6 years; boosters every 10 years.Treatment: antitoxin; erythromycin to prevent transmission immunization against diphtheria has shifted susceptibility to the disease to adolescents and adults. Immunity wanes after childhood because of lack of exposure to now scarce C. diphtheriae to boost immunity. To prevent buildup of a large population of susceptible older individuals, booster injections should be given every 10 years following childhood immunization.

Effective treatment of diphtheria depends on injecting antiserum against diphtheria toxin into the patient as soon as possible. If the disease is suspected, antiserum must be administered without waiting several days for culture results, because the delay could be fatal. The bacteria are sensitive to antibiotics such as erythromycin and penicillin, but such treatment only stops transmission of the disease; it has no effect on toxin that has already been absorbed. Even with treatment, about 1 of 10 diphtheria patients dies (range 3.5% to 22% depending on age, severity of disease, promptness of treatment, etc.).

Table 23.4 summarizes some important facts about diphtheria.

Pinkeye, Earache, and Sinus Infections

Bacterial infection of the eye's surface, generally known as conjunctivitis or "pinkeye," and infections of the middle ear (otitis media) and sinuses are very common, often occur together, and frequently have the same causative agent. This is not surprising in view of their intimate association with the nasal chamber and nasopharynx (see figure 23.1). Otitis media is a formidable problem, especially in children, responsible for 30 million doctor visits per year in the United States, at an estimated cost of $1 billion. Pinkeye, because of it high communicability, is a frequent source of panic when it appears in a day care facility or classroom. Sinusitis, inflammation of the sinuses, is common in both adults and children.

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Bacterial Vaginosis Facts

Bacterial Vaginosis Facts

This fact sheet is designed to provide you with information on Bacterial Vaginosis. Bacterial vaginosis is an abnormal vaginal condition that is characterized by vaginal discharge and results from an overgrowth of atypical bacteria in the vagina.

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