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Pathogenic cocci

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Chair of Microbiology, Virology, and Immunology
Pathogenic cocci
Staphylococci are included in the Firmicutes Bacteria,
family Micrococcaceae, genus Staphylococcus.
staphylococci are subdivided into more then 30 species.
Among them: S. aureus, S. epidermidis, and
S. saprophyticus, S. haemolyticus, S. capitis, S. hominis,
S. warneri, S. xylosus etc.
Staphylococci are spherical in
shape, 0.8-1 mcm in diameter, and
form irregular clusters resembling
bunches of grapes. In smears from
cultures and pus the organisms
occur in short chains, in pairs, or as
single cocci. Large spherical (Lforms) or very small (G-forms) and
even filterable forms may be seen in
cultures which have been subjected
to various physical, chemical, and
biological (antibiotics) factors.
Electron micrograph showing Staphylococcus
aureus morphology.
Staphylococci are
organisms which
possess no flagella
and do not form
Staphylococci are facultative-anaerobes.
They grow well on ordinary nutrient media with a pH of 7.2-7.4
at a temperature of 37 п‚°C but do not grow at temperatures below
10 п‚°C and above 45 п‚°C.
At room temperature with adequate aeration and subdued light –
the organisms produce golden, white, lemon-yellow, and other
pigments known as lipochromes. These pigments do not dissolve
in water but are soluble in ether, benzene, acetone, chloroform,
and alcohol.
On meat peptone agar Staphylococci produce well defined
colonies with smooth edges, measuring from 1-2 to 2.5 mm in
Growth of Staphylococci in meat-peptone broth produces diffuse
opacity throughout the medium and, subsequently, a precipitate. In
some cases when there is sufficient aeration, the organisms form a
pellicle on the surface of the broth. Staphylococci grow well on
potatoes and coagulated serum. After 24-48 hours of incubation
there is usually abundant growth along the inoculation stab and
liquefaction of gelatin media. On the fourth or fifth day the gelatin
medium resembles a funnel filled with fluid.
On blood agar pathogenic Staphylococci cause haemolysis
of the erythrocytes.
Antigenic structure.
Polysaccharide A was extracted from pathogenic strains isolated
from patients with septicaemia, furunculosis, osteomyelitis, and
acute conjunctivitis, etc.
Polysaccharide B is found in avirulent, non-pathogenic strains.
Polysaccharides A and B differ not only in their serological
reactions but also in their chemical structures.
Antigen C, containing a specific polysaccharide, has been
recently isolated.
The Virulence factors of Staphylococcus aureus
Pathogenesis and diseases in man.
Staphylococci enter the body through the skin and mucous
membranes. When they overcome the lymphatic barrier
and penetrate the blood, staphylococcal septicaemia sets in.
Both the exotoxins and the bacterial cells play an important
role in pathogenesis of diseases caused by these organisms.
Consequently, staphylococcal diseases should be regarded
as toxinfections.
The development of staphylococcal diseases is also
influenced by the resulting allergy which in many cases is
the cause of severe clinical forms of staphylococcal
infections which do not succumb to treatment.
Pathogenesis and diseases
May cause infection if the skin or mucous membranes are
broken or damaged. Staphylococci are responsible for a number of
local lesions in humans: hidradenitis, abscess, paronychia,
blepharitis, furuncle, carbuncle, periostitis, osteomyelitis, folliculitis,
sycosis, dermatitis, eczema, chronic pyodermia, peritonitis,
meningitis, appendicitis, and cholecystitis.
Staphylococcus aureus is considered the most pathogenic species,
causing abscesses, boils, carbuncles, acne, impetego, and less
commonly, pneumonia, osteomyelitis, endocarditis, cystitis,
pyelonephritis, and food poisoning.
Diabetes mellitus, avitaminosis, alimentary dystrophy,
excess perspiration, minor occupational skin abrasions, as well as
skin irritation caused by chemical substances, are some examples of
the conditions conducive to the formation of pyogenic lesions of the
skin and furunculosis.
Pathogenesis and diseases
In some cases staphylococci may give rise to secondary
infection in individuals suffering from smallpox, influenza,
and wounds, as well as postoperative suppurations.
Staphylococcal sepsis and staphylococcal pneumonia in
children are particularly severe diseases. Ingestion of
foodstuffs (cheese, curds, milk, rich cakes and pastry, ice
cream, etc.) contaminated with pathogenic staphylococci
may result in food poisoning.
Staphylococci play an essential part in mixed infections, and
are found together with streptococci in cases of wound
infections, diphtheria, tuberculosis, actinomycosis, and
Pathogenesis and diseases
The wide use of antibacterial agents, antibiotics in particular,
led to considerable changes in the severity and degree of the
spread of staphylococcal lesions. Growth in the incidence of
diseases and intrahospital infections in obstetrical, surgical
and children's in-patient institutions, intensive spread of the
causative agent, and increase in the number of carriers among
the medical staff and population have been noted in all
countries of the world. Intrauterine and extrauterine
contamination of children with staphylococci has been
registered, with the development of vesiculopustular
staphyloderma, pemphigus, infiltrates, abscesses, conjunctivitis,
nasopharyngitis, otitis, pneumonia, and other diseases.
The tendency to run a chronic flaccid course or relapse is
regarded as a characteristic symptom of staphylococcal
infections. This peculiarity gives a basis for concluding
that postinfectional immunity following staphylococcal
diseases is of low grade and short duration.
Immunity acquired after staphylococcal diseases is due
to phagocytosis and the presence of antibodies
(antitoxins, precipitins, opsonins, and agglutinins).
Laboratory diagnosis.
Test material may be obtained from pus,
mucous membrane discharge, sputum, urine, blood,
foodstuffs (cheese, curds, milk, pastry, cakes, cream,
etc.), vomit, lavage fluids, and faeces.
The material is examined for the presence of
pathogenic staphylococci. Special rules are observed
when collecting the material since non-pathogenic
strains are widespread in nature.
Identification of Gram Positive Cocci: Staphylococcus
Contains both pathogenic and nonpathogenic organisms
Do not produce endospores, but are
resistant to drying (desiccation)
Found routinely on the surface of the skin
Three major species:
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
The three species can be distinguished from
each other by various biochemical tests.
In this lab we will perform some of these
tests and observe the results.
S. epider- S. sapromidis
Protein A, superficial antigen
Production of
Resistance to
Coagulase Test
A zone of growth
inhibition 17 mm or
less in diameter
indicates resistance
(R) to Novobiocin.
If the zone is greater
than 11 mm the
organism is
susceptible (S) to
Treatment. Staphylococcal diseases are treated
with antibiotics (penicillin, phenoxymethyl penicillin,
(norsulphazol, sulphazol, etc.), and antistaphylococcal
Prophylaxis. The general precautionary measures include: hygiene in
working and everyday-life conditions, treatment of vitamin deficiency,
prevention of traumatism and excess perspiration, observance of rules of
hygiene in maternity hospitals, surgical departments, children's
institutions, industrial plants and enterprises, particularly canneries,
observance of personal hygiene and frequent washing of hands in warm
water with soap.
Routine disinfection of hospital premises (surgical departments, maternity
wards) and bacteriological examination of the personnel for carriers of
pathogenic staphylococci resistant to antibiotics are also necessary.
To prevent pyoderma protective ointments and pastes are used at
industrial enterprises. In some cases specific prophylaxis by means of
immunization with the staphylococcal anatoxin may be recommended for
individuals subject to injury or infection with antibiotic-resistant
Streptococci are spherical in shape, 0.6 to 1 mem in
diameter, and form chains. They are non-motile (although motile
forms are encountered), do not form spores and are Gram-positive.
Some strains are capsulated. In smears from cultures grown on
solid media the streptococci are usually present in pairs or in short
chains, while in smears from broth cultures they form long chains
or clusters.
Streptococci are facultatively aerobic, and there are also
anaerobic species. The optimal temperature for growth is 37В°
C, and no growth occurs beyond the limits of 20-40В° C for
enterococci the limits are 10-45 п‚°C).
The organisms show poor growth on ordinary meat-peptone
agar, and grow well on sugar, blood, serum and ascitic agar
and broth, when the pH of the media is 7.2-7.6. On solid
media they produce small (0.5-1.0 mm in diameter),
translucent, grey or greyish-white, and granular colonies with
poorly defined margins.
On sugar broth medium growth is in the form of fine-granular
precipitates on the walls and at the bottom of the tube and
only rarely does the broth become turbid.
Some streptococcal strains cause haemolysis on blood agar, others
produce a green coloration surrounding the colony 1-2 mm in
diameter as result a conversion of haemoglobin into
methaemoglobin, while others do not cause any change in the
Types of hemolysis
The Beta hemolysis:
The alpha hemolysis:
The Gamma ( non hemolytic)
Fermentative properties. Streptococci are nonproteolytic, do not liquefy gelatin, and do not reduce nitrates
to nitrites. They coagulate milk, dissolve fibrin, ferment
glucose, maltose, lactose, saccharose, mannitol (not always
constantly), and break down salicin and trehalose, with acid
Classification. By means of the precipitation reaction
founded on the detection of group specific carbohydrates,
streptococci are subdivided into groups which are designated
by capital letters from A to H and from K to T.
Five out of the 21 known Streptococcal species cannot be
related to any antigenic group. Nine species are of interest for
medical microbiology;
The haemolytic streptococci, recovered from sick
human beings, were subdivided by F. Griffith into 51
serovars. He attributed 47 serovars to group A, serovars 7, 20,
and 21 to group C, and serovar 16 to group G.
Pathogenesis and diseases in man. The pathogenesis of
streptococcal infections is brought about by the effect of the
exotoxin and the-bacterial cells.The reactivity of the infected
body and its previous resistance play an important part in the
origin and development of streptococcal diseases. Such
diseases as endocarditis, polyarthritis, highmoritis, chronic
tonsillitis, and erysipelas are associated with abnormal body
reactivity, hyperergia. This condition may persist for a long
period of time and serve as the main factor for the
development of chronic streptococcal diseases.
With an exogenous mode of infection streptococci invade the
human body from without (from sick people, and animals,
various contaminated objects and foodstuffs).
They gain access through injured skin and mucous
membranes or enter the intestine with the food. Streptococci
are mainly spread by the air droplet route. When the
natural body resistance is weakened, conditionally pathogenic
streptococci normally present in the human body become
Penetrating deep into the tissues they produce local pyogenic
streptoderma, abscesses,
phlegmons, lymphadenitis, lymphangitis, cystitis, pyelitis,
cholecystitis, and peritonitis. Erysipelas (inflammation of
the superficial lymphatic vessels) and tonsillitis
(inflammation of the pharyngeal and tonsillar mucosa) are
among the diseases caused by streptococci. Invading the
blood, streptococci produce a serious septic condition. They
are more commonly the cause of puerperal sepsis than other
Streptococci may cause secondary infections in patients with
diphtheria, smallpox, whooping cough, measles, and other
diseases. Chronic tonsillitis is attributed to the viridans
streptococci and adenoviruses. Contamination of wounds
with streptococci during war results in wound suppurations,
abscess formation, phlegmons, and traumatic sepsis.
Role of Streptococcus in the Aetiology of Scarlet Fever
Scarlet fever has long been known as a widespread disease but
at the present time its aetiology has not yet been ascertained.
Four different theories were proposed: streptococcal, allergic,
viral, and combined (viral-streptococcal). Most scientists and
medical practitioners favoured the streptococcal theory.
It is assumed that scarlet fever is caused by group A betahaemolytic streptococci which possess M-antigen and produce
erythrogenic exotoxin. People become infected by the air
droplet route. Sic k people, convalescents, and carriers of the
causative agent of scarlet fever are all sources of infection. The
disease is most commonly encountered in children from 1 to 8
years of age.
The causative agent sometimes enters the body through
wounds on the skin and mucous membranes of the
genitalia. This form of scarlet fever is known as
extrabuccal or extrapharyngeal (traumatic, combustion,
surgical, and puerperal). Certain objects (e. g. utensils,
toys, books, etc.) as well as foodstuffs (e. g. milk),
contaminated by adult carriers, may also be sources of
infection. Of great importance in the epidemiology of
scarlet fever are the patients with atypical,
unrecognizable forms of the disease. In its initial stage
scarlet fever is chiefly characterized by intoxication,
while in the second stage it is accompanied by septic
and allergic conditions.
Immunity. Immunity acquired after streptococcal infections
is ofa low grade and short duration. Relapses of erysipelas,
fre quent tonsilitis, dermatitis, periostitis, and osteomyelitis
occur as a result of sensitization of the body. This is
attributed to low immunogenic activity and high allergen
content of the streptococci, as well as to the presence of
numerous types of the organisms against which no cross
immunity is produced.
Immunity following streptococcal infections is of an antiinfectious nature. It is associated with antitoxic and
antibacterial factors. The antitoxins neutralize the
streptococcal toxin and together with the opsonins facilitate
Laboratory diagnosis. Test material is obtained from
the pus of wounds, inflammatory exudate. tonsillar swabs,
blood, urine, and foodstuffs. Procedures are the same as for
staphylococcal infections. Tests include microscopy of pus
smears, inoculation of test material onto blood agar plates,
isolation of the pure culture and its identification. Blood is
sown on sugar broth if sepsis is suspected. Virulence is tested
on rabbits by an intracutaneous injection of 200-400 million
microbial cells. Toxicity is determined by injecting them
intracutaneously with broth culture filtrate.
The group and type of the isolated streptococcus and its
resistance to the medicaments used are also determined. In
endocarditis there are very few organisms present in the blood
in which they appear periodically. For this reason blood in
large volumes (20-50 ml) is inoculated into vials containing
sugar broth. If possible, the blood should be collected while
the patient has a high temperature. In patients with chronic
sepsis an examination of the centrifuged urine precipitate and
isolation of the organism in pure culture are recommended.
Besides, the group and type of the isolated streptococcus are
identified by means of fluorescent antibodies. Serological
methods are also applied to determine the increase in the titre
of antibodies, namely streptolysins O and antihyaluronidase.
Treatment. Usually penicillin is used. For penicillinresistant strains,and when penicillin is contraindicated,
streptomycin, and erythromycin are required. Vaccine
therapy (autovaccines and polyvalent vaccines) and phage
therapy are recommended in chronic conditions.
In some countries diseases caused by beta-haemolytic
streptococci of groups A, C, G, and H and by alphastreptococci (endocarditis) are treated with anti-infectious
(antitoxic and antibacterial) streptococcal sera together with
antibiotics and sulphonamides.
Prophylaxis. Streptococcal infections are prevented by the
practice of general hygienic measures at factories, children's
institutions, maternity hospitals, and surgical departments, in
food production, agricultural work, and everyday life.
Maintaining appropriate sanitary levels of living and working
condi- tions, raising the cultural level of the population, and
checking personal hygiene are of great importance.
Since streptococci and the macro-organism share antigenic
structures in common and because streptococci are marked
by weak immunogenic ability and there are a great number of
types among them which do not possess the property of
producing cross immunity, specific prophylaxis of
streptococcal diseases has not been elaborated. Vaccines
prepared from M-protein fractions of streptococci are being
The meningococcus (Neisseria meningitidis) was
isolated from the cerebrospinal fluid of patients with
meningitis and studied in detail in 1887 by A.
Weichselbaum. At present the organism is classified in
the genus Neisseria, family Neisseriaceae
Morphology. The meningococcus is a coccus 0.6-1 mcm
in diameter, resembling a coffee bean, and is found in
pairs (fig. 1). The organism is Gram-negative. As distinct
longitudinally by their concave edges while their external
sides are convex. Spores, capsules and flagella are not
formed. In pure cultures meningococci occur as tetrads
(in fours) and in pus they are usually found within and
less frequently outside the leukocytes. The G+C content
in DNA ranges from 50.5 to 51.3 per cent. In culture
smears, small or very large cocci are seen singly, in pairs,
or in fours. Meningococci may vary not only in shape but
also in their Gram reaction. Gram-positive diplococci
appear among the Gram-negative cells in smears.
Cultivation. The meningococcus is an aerobe or facultative
anaerobe and does not grow on common media. It grows readily at pH
7.2-7.4 on media to which serum or ascitic fluid has been added.
Optimum temperature for growth is 36-37 п‚°C and there is no growth at
22В° C.
Microbiologists use a peptone-blood base medium in a moist
chamber containing 5-10 % CO2. All media must be warmed to 37
degrees prior to inoculation as the organism is extremely susceptible
to temperatures above or below 37 degrees.
On solid media the organisms form fine transparent colonies
measuring 2-3 mm in diameter. In serum broth they produce turbidity
and a precipitate at the bottom of the test tube, and after 3-4 day's, a
pellicle is formed on the surface of the medium.
Meningococci can be adapted to simple media by repeated
subculture on media with a gradual change from the optimum protein
concentration to media containing a minimal concentration of proteins.
Fermentative properties. Meningococci do not liquefy
gelatin, cause no change in milk, and ferment glucose and maltose,
with acid formation.
Toxin production. Meningococci produce toxic substances
which possess properties of exo- and endotoxins. Disintegration of
bacterial cells leads to the release of a highly toxic endotoxin.
Meningococci readily undergo autolysis which is accompanied by
accumulation of toxins in the medium. The meningococcal toxin is
obtained by treating the bacterial cells with distilled water, or 10 N
solution of soda, by heat autolysis, by exposure to ultraviolet rays.
Major toxin of N. meningitidis is its lipooligosaccharide,
LOS, and its mechanism is endotoxic.
The other important determinant of virulence of N.
meningitidis is its antiphagocytic polysaccharide capsule.
Fimbriae are factor of virulence
Antigenic structure and classification. Meningococci were found
to contain three fractions: carbohydrate (C) which is common to all
meningococci, protein (P) which is found in gonococci and type III
S. pneumoniae, and a third fraction with which the specificity of
meningococci is associated.
According to the International Classification Twelve groups of
meningococci are distinguished, groups A, B, C, D, H, I, K, L, X, Y,
Z, 29E, and W135.
Types A, B, C, Y, and W135 are dominant.
The organisms are characterized by intraspecies variability. A
change of types takes place at certain times.
Pathogenesis and diseases in man. People suffering from
meningococcal infection and carriers are sources of diseases. The
infection is transmitted by the air-droplet route. The causative agent is
localized primarily in the nasopharynx. From here it invades the lymph
vessels and blood and causes the development of bacteriemia. Then as a
result of metastasis the meningococci pass into the meninges and
produce acute pyogenic inflammation in the membranes of the brain and
spinal cord (nasopharyngitis, meningococcaemia, meningitis).
The disease usually arises suddenly with high temperature,
vomiting, rigidity of the occipital muscles, severe headache, and
increased skin sensitivity. Later paresis of the cranial nerves develops
due to an increase in the intracranial pressure. Dilatation of the pupils,
disturbances of accommodation, as well as other symptoms appear. A
large number of leukocytes are present in the cerebrospinal fluid, and the
latter after puncture escapes with a spurt because of the high pressure.
In some cases meningococcal sepsis develops. In such conditions
the organisms are found in the blood, joints, and lungs. The disease
mainly attacks children from 1 to 5 years of age. Before the use of
antibiotics and sulphonamides the death rate was very high (30-60 per
The population density plays an important part in the spread of
meningitis. During epidemic outbreaks there is a large number of carriers
for every individual affected by the disease. In non-epidemic periods the
carrier rate increases in the spring and autumn. Body resistance and the
amount and virulence of the causative agent are significant. Depending
on these factors, the spread of infection is either sporadic or epidemic.
Meningitis can also be caused by other pathogenic microbes
(streptococci, E. coli, staphylococci, bacteria of influenza, mycobacteria
of tuberculosis, and certain viruses). These organisms, however, cause
sporadic outbreaks of the disease, while meningococci may cause
epidemic meningitis.
Immunity. There is a well-developed natural immunity
in humans. Acquired immunity is obtained not only as a result
of the disease but also as the result of natural immunity
developed during the meningococcal carrier state. In the
course of the disease agglutinins, precipitins, opsonins, and
complement-fixing antibodies are produced. Recurring
infections are rare.
Laboratory diagnosis. Specimens of
cerebrospinal fluid, nasopharyngeal discharge,
blood, and organs obtained at autopsy are used for
The following methods of investigation are
employed: (1) microscopic examination of
cerebrospinal fluid precipitate; (2) inoculation of
this precipitate, blood or nasopharyngeal
discharge into ascitic broth, blood agar, or ascitic
agar; identification of the isolated cultures by their
differentiation of meningococci from the catarrhal
micrococcus (Branhamella catarrhalis) and
saprophytes normally present in the throat. The
meningococcus ferments glucose and maltose,
whereas Branhamella catarrhalis does not
ferment carbohydrates, and Neisseria sicca
ferments glucose, levulose, and maltose; (3)
performance of the precipitin reaction with the
cerebrospinal fluid.
Treatment. Antibiotics (penicillin, oxytetracycline, etc.) and
sulphonamides (streptocid, methylsulphazine) are prescribed.
Prophylaxis is ensured by general sanitary procedures and
epidemic control measures (early diagnosis, transference of
patients to hospital), appropriate sanitary measures in relation
to carriers, quarantine in children's institutions. Observance of
hygiene in factories, institutions public premises, and
lodgings, and prevention of crowded condition are also
obligatory. An antimeningococcal vaccine derived from the
C/B serogroup is now under test. It contains specific
The incidence of meningitis has grown recently. The disease
follows a severe course and sometimes terminates in death.
The causative agent of gonorrhoea and blennorrhoea
(Neisseria gonorrhoeae) was discovered in 1879 by A.
Neisser in suppurative discharges. In 1885 E. Bumm isolated
a pure culture of the organism and studied it in detail.
Gonococci belong to the genus Neisseria, family
Morphology. Gonococci are morphologically similar
to meningococci. The organism is a paired, bean-shaped
coccus, measuring 0.6-1 mcm in diameter. It is Gramnegative and occurs inside and outside of the cells. Neither
spores nor flagella are formed. Under the electron
microscope a cell wall, 0.3-0.4 mcm in thickness,
surrounding the gonococci is visible. The G+C content in
DNA is 49.5 to 49.6 per cent.
Pleomorphism of the gonococci is a characteristic property.
They readily change their form under the effect of
medicines, losing their typical shape, and growing larger,
sometimes turning Gram-positive, and are found outside
the cells.
In chronic forms of the disease autolysis of the gonococci
takes place with formation of variant types (Asch types).
Usually gonococcal cells varying in size and shape are
formed. The tendency toward morphological variability
among the gonococci should be taken into account in
laboratory diagnosis. L-forms occur under the effect of
Cultivation. The gonococcus is an aerobe or facultative
anaerobe which does not grow on ordinary media, but can be
cultivated readily on media containing human proteins (blood,
serum, ascitic fluid) when the pH of the media is in the range
of 7.2-7.6. The optimum temperature for growth is 37В° C, and
the organism does not grow at 25 and 42В° C. It also requires an
adequate degree of humidity. Ascitic agar, ascitic broth, and
egg-yolk medium are the most suitable media. On solid media
gonococci produce transparent, circular colonies, 1-3 mm in
diameter. Cultures of gonococci form a pellicle in ascitic
broth, which in a few days settles at the bottom of the test
Fermentative properties. The gonococcus possesses
low biochemical activity and no proteolytic activity. It
ferments only glucose, with acid formation.
Toxin production. The gonococci do not produce
soluble toxin (exotoxin) An endotoxin is released as a result of
disintegration of the bacterial cells. This endotoxin is also
toxic for experimental animals.
Antigenic structure and classification. The antigenic
structure of gonococci is associated with the protein (Oantigen) and polysaccharide (K-antigen) fractions. No group
specific or international types of gonococci have been
revealed. Gonococci and meningococci share some antigens in
Surface components of N. gonorrhoeae that may play a role in virulence
Major fimbrial
P.II (Opa)
Outer membrane
Contributes to invasion
P.I (Por)
Outer membrane
May prevent phagolysosome
formation in neutrophils
and/or reduce oxidative burst
Outer membrane
Elicits inflammatory response,
triggers release of TNF
P.III (Rmp)
Outer membrane
Elicits formation of ineffective
antibodies that block that
block bactercidal antibodies
against P.I and LOS
and Outer membrane
Iron acquisition for growth
Outer membrane
receptor for
Iron acquisition for growth
receptors for
Pathogenesis and diseases in man. Patients with gonorrhoea are
sources of the infection. The disease is transmitted via the genital organs
and by articles of domestic use (diapers, sponges, towels, etc). The
causative agent enters the body via the urethral mucous membranes and,
in women, via the urethra and cervix uteri. Gonorrhoea is accompanied
by acute pyogenic inflammation of the urethra, cervix uteri, and glands
in the lower genital tract. Often, however, the upper genito-urinary
organs are also involved. Inflammations of the uterus, uterine tubes, and
ovaries occur in women, vulvovaginitis occurs in girls, and inflammation
of the seminal vesicles and prostata in men. The disease may assume a
chronic course. From the cervix uteri the gonococci can penetrate into
the rectum. Inefficient treatment leads to affections of the joints and
endocardium, and to septicaemia. Gonococci and Trichomonas vaginalis
are often found at the same time in sick females. The trichomonads
contain (in the phagosomes) gonococci protected by membranes against
the effect of therapeutic agents. Gonococcus is responsible for
gonorrhoeal conjunctivitis and blennorrhea in adults and newborn
Immunity. The disease does not produce
insusceptibility and there is no congenital immunity.
Antibodies (agglutinins, precipitins, opsonins, and
complement-fixing bodies) are present in patients' sera,
but they do not protect the body from reinfection and
recurrence of symptoms. Phagocytosis in gonorrhoea is
incomplete. The phagocytic and humoral immunity
produced in gonorrhoea is incapable of providing
complete protection, so, in view of this fact, treatment
includes measures which increase body reactivity. This is
achieved by raising the patient's temperature artificially.
Laboratory diagnosis. Specimens for microscopic
examination are obtained from the discharge of the urethra,
vagina, vulva, cervix uteri, prostate, rectal mucous
membrane, and conjunctiva. The sperm and urine
precipitates and filaments are also studied microscopically,
Smears are stained by Gram's method and with methylene
blue by Loeffler's method). Microscopy is quite frequently
an unreliable diagnostic method since other Gram-negative
bacteria, identical to the gonococci, may be present in the
material under test. Most specific are the immunofluorescence methods (both direct and indirect). In the direct
method the organisms under test are exposed to the action of
fluorescent antibodies specific to gonococci. In the indirect
method, the known organisms (gonococci) are treated with
patient's serum. The combination of the antibody with the
antigen becomes visible when fluorescent antiserum is
Laboratory diagnosis. If diagnosis cannot be made
by microscopic examination, isolation of the culture is
carried out. For this purpose the test material (pus,
conjunctival discharge, urine precipitate, etc.) is inoculated
onto media. The Bordeux-Gengou complement-fixation
reaction and the allergic test are employed in chronic and
complicated cases of gonorrhea.
Treatment. Patients with gonorrhoea are prescribed
antibiotics (bicillin-6, ampicillin, monomycin, kanamycin)
and sulphonamides of a prolonged action. Injections of
polyvalent vaccine and autovaccine as well as pyrotherapy
(introduction of heterologous proteins) are applied in
complicated cases.
Improper treatment renders the gonococci drug-resistant, and
this may lead to the development of complications and to a
chronic course of the disease.
Prophylaxis includes systematic precautions for
establishing normal conditions of everyday and family life,
health education and improvement of the general cultural
and hygienic standards of the population.
In the control of gonorrhoea great importance is assigned
to early exposure of sources of infection and contacts and
to successful treatment of patients.
The prevention of blennorrhea is effected by introducing
one or two drops of a 2 per cent silver nitrate solution into
the conjunctival sac of all newborn infants. In certain cases
(in prematurely born infants) silver nitrate gives no
positive result. Good results are obtained by introducing
two drops of a 3 per cent penicillin solution in oil into the
conjunctival sac. The gonococci are killed in 15-30
In spite of the use of effective antibiotics the incidence of
gonorrhoea tends to be on the increase in all countries
(Africa, America, South-Eastern Asia, Europe, etc.). The
number of complications has also increased: gonococcal
ophthalmia of newborn infants (blennorrhea),
vulvovaginitis in children, and inflammation of the
pelvic organs (salpingitis) and sterility in women. The
rise in the incidence of gonorrhoea is caused by social
habits (prostitution, homosexualism, etc.), inefficient
registration of individuals harbouring the disease,
deficient treatment, and the appearance of gonococci
resistant to the drugs used.
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