Microbiology

Lesson VI
LISTERIA MONOCYTOGENES
The genus Listeria consists of 10 species, with Listeria monocytogenes and Listeria ivanovii
the only recognized pathogens. L. monocytogenes is a significant human pathogen, and L.
ivanovii is primarily an animal pathogen. L. monocytogenes is a short, gram-positive,
facultatively anaerobic rod capable of growth at a broad temperature range (1° C to 45° C)
and in a high concentration of salt.
L. monocytogenes is isolated from a variety of environmental sources and from the feces of
mammals, birds, fish, and other animals. The primary source of infection with this organism
is consumption of contaminated food; however, human to human transmission can occur
primarily from mother to child in utero or at birth. Fecal carriage is estimated to occur in 1%
to 5% of healthy people.
Clinical Diseases
Neonatal Disease
Two forms of neonatal disease have been described: (1) early-onset disease, acquired
transplacentally in utero, and (2) late-onset disease, acquired at or soon after birth. Early-
onset disease can result in abortion, stillbirth, or premature birth. Granulomatosis
infantiseptica is a severe form of early-onset listeriosis, characterized by the formation of
abscesses and granulomas in multiple organs and a high mortality rate unless treated
promptly. Late-onset disease occurs 2 to 3 weeks after birth, in the form of meningitis or
meningoencephalitis with septicemia. The clinical signs and symptoms are not unique; thus
other causes of neonatal central nervous system disease, such as group B streptococcal
disease, must be excluded.
Meningitis in Adults
Meningitis is the most common form of disseminated Listeria infection in adults. Although
the clinical signs and symptoms of meningitis caused by this organism are not specific,
Listeria should always be suspected in patients with organ transplants or cancer and in
pregnant women in whom meningitis develops. Disease is associated with a high mortality
(20% to 50%) and significant neurologic sequelae among the survivors.
Treatment, Prevention, and Control
Because most antibiotics are only bacteriostatic with L. monocytogenes, the combination of
gentamicin with either penicillin or ampicillin is the treatment of choice for serious
infections. Listeriae are naturally resistant to cephalosporins, and resistance to macrolides,
fluoroquinolones, and tetracyclines has been observed, which can limit the utility of these
drugs.
Because listeriae are ubiquitous (everywhere) and most infections are sporadic (irregular),
prevention and control are difficult. People at high risk of infection should avoid eating raw
or partially cooked foods of animal origin and unwashed raw vegetables. A vaccine is not
available, and prophylactic antibiotic therapy for high-risk patients has not been evaluated.

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CORYNEBACTERIUM DIPHTHERIAE

Corynebacteria are ubiquitous in plants and animals, and they normally colonize the skin,
upper respiratory tract, gastrointestinal tract and urogenital tract in humans. Although all
species of corynebacteria can function as opportunistic pathogens, relatively few are
associated with human disease. The most famous of these is Corynebacterium
diphtheriae, the etiologic agent of diphtheria.

Diphtheria is a disease found worldwide, particularly in poor urban areas where there is
crowding and the protective level of vaccine-induced immunity is low. C. diphtheriae is
maintained in the population by asymptomatic carriage in the oropharynx or on the skin
of immune people. Respiratory droplets or skin contact transmits it from person to
person. Humans are the only known reservoir for this organism.

Clinical Diseases
The clinical presentation of diphtheria is determined by;
(1) the site of infection,
(2) the immune status of the patient,
(3) the virulence of the organism.

Exposure to C. diphtheriae may result in asymptomatic colonization in fully immune

people, mild respiratory disease in partially immune patients, or a fulminant, sometimes
fatal, disease in nonimmune patients. Diphtheria toxin is produced at the site of the
infection and then disseminates through the blood to produce the systemic signs of
diphtheria. The organism does not need to enter the blood to produce disease.

Respiratory Diphtheria
The symptoms of diphtheria involving the respiratory tract develop after a 2- to 4-day
incubation period. Organisms multiply locally on epithelial cells in the pharynx or
adjacent surfaces and initially cause localized damage as a result of exotoxin activity.
The onset is sudden, with malaise, sore throat, exudative pharyngitis, and a low-grade
fever. The exudate evolves into a thick pseudomembrane composed of bacteria,
lymphocytes, plasma cells, fibrin, and dead cells that can cover the tonsils, uvula, and
palate and can extend up into the nasopharynx or down into the larynx . The
pseudomembrane firmly adheres to the underlying tissue and is difficult to dislodge
without making the tissue bleed (unique to diphtheria). As the patient recovers after the
approximately 1-week course of the disease, the membrane dislodges and is
expectorated. Systemic complications in patients with severe disease primarily involve
the heart and nervous system. Evidence of myocarditis can be detected in the majority of
patients with diphtheria, typically developing 1 to 2 weeks into the illness and at a time
when the pharyngeal symptoms are improving. Symptoms can present acutely or
gradually, progressing in severe disease to congestive heart failure, cardiac arrhythmias,
and death. Neurotoxicity is proportional to the severity of the primary disease, which is
influenced by the patient’s immunity. The majority of patients with severe primary
disease develop neuropathy, initially localized to the soft palate and pharynx, later
involving oculomotor and ciliary paralysis, with progression to peripheral neuritis.

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Cutaneous Diphtheria
Cutaneous diphtheria is acquired through skin contact with other infected persons. The
organism colonizes the skin and gains entry into the subcutaneous tissue through breaks
in the skin. A papule develops first and then evolves into a chronic, nonhealing ulcer,
sometimes covered with a grayish membrane. Staphylococcus aureus or Streptococcus
pyogenes is also frequently present in the wound.

Treatment, Prevention, and Control

The most important aspect of the treatment for diphtheria is the early administration of
diphtheria antitoxin to specifically neutralize the exotoxin before it is bound by the host
cell. Once the cell internalizes the toxin, cell death is inevitable. Unfortunately, because
diphtheria may not be suspected initially, significant progression of disease can occur
before the antitoxin is administered.
Antibiotic therapy with penicillin or erythromycin is also used to eliminate C. diphtheriae
and terminate toxin production.

Bed rest, isolation to prevent secondary spread, and maintenance of an open airway in
patients with respiratory diphtheria are all important. After the patient has recovered,
immunization with toxoid is required because most patients fail to develop protective
antibodies after a natural infection. Symptomatic diphtheria can be prevented by actively
immunizing people with diphtheria toxoid. The nontoxic, immunogenic toxoid is
prepared by formalin treatment of the toxin. Initially, children are given five injections of
this preparation with pertussis and tetanus antigens (DPT vaccine)