Download Bacteriology Dr. Zainab Adil Chabuck Bordetella

Bacteriology
Dr. Zainab Adil Chabuck
Bordetella
Bordetella genus comprises five species, four of which cause infections of the upper respiratory
tract in different host organisms. Bordetella pertussis is an obligate human pathogen and the only
organism of major clinical significance within this genus; it causes whooping cough in infants and
young children. A closely related organism, B. parapertussis can also cause a milder form of
bronchitis. B. bronchosepticus, another member, is the causative agent of respiratory diseases in
cats and swine, but can cause broncho-pulmonary symptoms in severely immunosupressed
individuals.
Bordetella pertussis
Morphology and physiology:- is a small Gram-negative coccobacillus. It is aerobic and grows best
at 35-37°C. Bordetella species, including B. pertussis and B. parapertussis, are fastidious and
difficult to grow on ordinary media. B. pertussis requires supplemental growth factors including
charcoal, blood, and starch. Media such as Bordet-Gengou, which contains potato starch, and
charcoal-based media typically are used for culturing the organism. B. pertussis is oxidase positive
but urease negative, while B. parapertussis is oxidase negative and urease positive. B.
bronchosepticus is positive for both enzymes.
Epidemiology:- Whooping cough (Pertussis) is a worldwide infectious disease caused by
Bordetella pertussis. It is a respiratory disease occurring after transmission of the bacteria from
person-to-person in airborne droplets expelled by severe coughing. Since no animal reservoir for B.
pertussis, the bacterium appears unable to survive in the environment for long periods of time. The
bacteria are highly infectious and unprotected close-contacts are liable to become infected. The
severity of disease is also age-related. Incidence is highest in children under five, except where
infant vaccination programs have been effective.
Pathogenesis:- The symptoms following the infection are due to many factors. In addition to the
attachment to and growth on bronchial ciliary epithelial cells, invades alveolar macrophages,
multiplies rapidly on the mucous membrane; the organism produces a number of exotoxins which
contribute to these symptoms.
Pertussis toxin:- PT is an oligopeptide AB-type exotoxin that is the major cause of pertussis
(abnormal cough). It causes T cell lymphocytosis and has an adjuvant properties. It also contributes
to bacterial binding to ciliated epithelial cells and the accumulation of large amounts of cAMP
which leads to increased mucus secretion and interferes with many cellular functions.
Adenylate cyclase toxin: This exotoxin penetrates the host cells, catalyzes the conversion of ATP
to cAMP. Like PT, it also inhibits phagocyte and NK cell functions. However, in contrast with PT,
the cAMP increase caused by this toxin is short-lived.
Tracheal cytotoxin: binds to ciliated epithelial cells, thus interfering with ciliary movement. In
higher concentrations, it causes ciliated epithelial cell extrusion and destruction. The destruction of
these cells contributes to pertussis.
Dermonecrotic (heat-labile) toxin: is a very strong vaso-constrictor and causes ischemia and
extravasation of leukocytes and, in association with tracheal cytotoxin, causes necrosis of the
tracheal tissue.
Filamentous haemagglutinins (agglutinogens): These are not exotoxins but are filamentassociated lipooligosaccharides which are implicated in the binding of the organism to ciliated
epithelial cells. Antibodies against these molecules are protective, probably by preventing bacterial
attachment.
Lipopolysaccharide (LPS): Like LPS of other gram negative bacteria, these endotoxins cause a
number of patho-physiolocigal effects. When released in relatively large quantities following
bacterial cell lysis, they cause irreversible shock and cardiovascular collapse. In smaller quantities,
they activate a variety of inflammatory mediators (TNF, IL1, IL6, prostaglandins, etc.) and generate
complement activation products.
Clinical Symptoms: The disease typically lasts 6 to 12 weeks or longer with three stages: catarrhal,
paroxysmal and convalescent. A child suspected of having pertussis should be placed in an
appropriate isolation until the infection is confirmed or ruled out.
-Catarrhal Phase: It lasts from 1 to 2 weeks and includes nonspecific complaints. Mild fever,
cough, sneezing, rhinitis and other flu-like symptoms, which often leads to a delay in identifying
suspected cases. During this phase of the illness, the cough worsens as the patient progresses to the
paroxysmal phase.
-Paroxysmal phase: It lasts from week 2 to 6. This phase is characterized by paroxysms of cough,
as many as 5 to 10 uninterrupted coughs occur in series, followed by a “whoop” as the patient
rapidly draws in a breath. The paroxysms may occur several times per hour and can be associated
with cyanosis, salivation, lacrimation, and post-tussive emesis. These paroxysms can be exhausting
and often interfere with sleep and nutritional intake. Patients often appear relatively well between
episodes.
-Convalescent Phase: Following the peak of the paroxysmal phase, improvement in respiratory
tract integrity and function is associated with decreasing frequency and severity of the coughing
episodes. The duration of this convalescent phase is highly variable, lasting from weeks to months.
- apnea, pneumonia, otitis media, meningo-encephalitis, seizures, encephalopathy, rectal prolapse
and death are among the secondary complications.
Diagnosis:
Symptoms are characteristic. Laboratory diagnosis is made by obtaining a nasopharyngeal aspirate
and primary culture on Bordet-Gengou. The organism grows as small transparent hemolytic
colonies. It can be serologically distinguished from B. parapertussis and B. bronchosepticus.
Prevention and treatment:
A killed whole bacterial vaccine is normally administered as DPT combination. An acellular
vaccine consisting of filamentous hemagglutinins and detoxified pertussis-gene is also available and
is recommended for booster shots. Erythromycin is the current drug of choice.
Brucella
Brucella cause disease primarily in domestic, wild animals and also pathogenic for animal and
cause abortion. It’s a true zoonotic, as all human infections are acquired from animal, humans is
considered as an accidental host.
General characteristics: Brucella genus are Gram-negative, facultative intracellular, nonmotile,
aerobic coccobacilli. Rough colony morphology when grown on artificial medium, as it need
selective media enrich with animal serum and glucose, with 5-10% carbon dioxide and prolong
incubation period.
Classification: The genus Brucella consists of six recognized species based on antigenic/
biochemical characteristics and primary host species, among them three species known to cause
disease in humans; B. abortus (cattle), B. melitensis (sheep and goats), B. suis (swine).
B. melitensis is thought to be the most virulent and causes the most severe and acute cases of
brucellosis. It is also the most prevalent worldwide. A prolonged course of illness, often associated
with suppurative destructive lesions, is associated with B suis infections. B abortus is associated
with mild-to-moderate sporadic disease that rarely causes complications.
Transmission: Brucellosis is a zoonotic disease and transmitted from animals to humans in several
ways. Most common route of transmission occurs when humans consume raw milk or cheese from
infected sheep and goats. Infected animals shed the organism into their milk, and if humans eat or
drink unpasteurized dairy products from these affected animals, they may develop brucellosis.
Other routes of infection include direct inoculation through cuts and abrasions in the skin,
inhalation of infectious aerosols.
Blood transfusion, tissue transplantation and sexual transmission are possible but rare routes of
infection.
Pathogenesis: Brucella species are facultative intracellular bacteria that can multiply within
phagocytic cells with human beings as end hosts. a few organisms (10 to 100) being sufficient to
cause a debilitating chronic infection.
After infecting the host, pathogen becomes sequestered within cells of the reticuloendothelial
system (liver, spleen and B. marrow) via hematogenous dissemination, then evades intracellular
killing, penetrate host cells, alter intracellular trafficking to avoid degradation and killing in
lysosomes, and modulate the intracellular environment to allow long-term intracellular survival and
replication.
If condition not controlled locally, infection progresses with the formation of small granulomas in
the reticuloendothelial sits of bacterial multiplication and with release of bacteria back into the
systemic circulation. These bacteremic episodes are responsible for the recurrent chills and fever of
the clinical illness.
In animal infection usually establishes itself in the reproductive tract and erythritol present in
placental tissue stimulates growth of Brucella. The human placenta does not contain erythritol.
Thus, in contrast to animals, abortion is not a feature of brucellosis in pregnant women.
Clinical disease: Brucellosis=Malta fever=Mediterranean fever=Undulant fever.
The disease is acute in about half the cases, with an incubation period of two to three weeks.
In the other half, the onset is insidious, with signs and symptoms developing over a period of weeks
to months from the infection. The clinical manifestations are varied and nonspecific. They include
fever, sweats, fatigue, malaise, anorexia, weight loss, headache, arthralgia and back pain.
Commonly, patients feel better in the morning, with symptoms worsening as the day progresses.
The desire to rest can be profound, and depression is common. If untreated, the pattern of the fever
that reach 38-40°C with pattern of waxes and wanes over several days (“undulant fever”).
Enlargement of the liver, spleen and/or lymph nodes may occur, as may signs referable to
almost any other organ system. Most people with this undulant form recover completely in three to
12 months. A few patients become chronically ill. Relapses can occur months after the initial
symptoms, even in successfully treated cases.
Diagnosis:1- Biopsy and blood culture are most definite method for diagnosis of brucellosis
2- Serological test such as Rose-Bengal test
3- Skin test (brucellin test) is positive especially in chronic cases
Treatment:Doxycycline in combination with an aminoglycoside (streptomycin or gentamycin) is the
primary treatment. Rifampicin, ciprofloxacin, and trimethoprim-sulphamethoxazole.