7.systemic Bacteriology

Systemic bacteriology
Shimelis Teshome (BSc MLS)

Gram Positive Cocci
1. Staphylococci
Physiology and morphology
• Staphylococci are nonmotile, catalase-
producing bacteria.
• Staphylococci are Gram-positive cocci
occurring in clusters.
• The genus Staphylococcus includes over 30
species and subspecies.
02/23/2021 Shimelis Teshome (BSc MLS) 2
• The most important species from the viewpoint
of human medicine is S. aureus.
• A number of extracellular enzymes and
exotoxins such as coagulase, alphatoxin,
leukocidin, exfoliatins, enterotoxins, and toxic
shock toxin are responsible for the clinical
symptoms of infections by this pathogen
• Laboratory diagnosis involves identification of
the pathogen by means of microscopy and
culturing.

Staphylococcus
• Coagulase-negative staphylococci are classic
opportunistc.
• S. epidermidis and other species are frequent agents
in foreign body infections due to their ability to
form biofilms on the surfaces of inert objects.
• S. saprophyticus is responsible for between 10 and
20% of acute urinary tract infections in young
women.
Furuncles in a patient with type 2 diabetes mellitus.

2. Streptococcus and Enterococcus
• Streptococci are Gram-positive, nonmotile,
catalase-negative, facultatively anaerobic cocci
that occur in chains or pairs.
• They are classified based on their hemolytic
capacity (α, β, γ-hemolysis) and the antigenicity
of a carbohydrate occurring in their cell walls
(Lancefield antigen).
A. Gram staining of pleural puncture
biopsy material: gram-positive
cocci in twisted chains.
B. Culture on blood agar: small,

whitish-gray colonies surrounded
by large β-hemolysis zones; a 5%
CO2 atmosphere provides optimum
conditions for β- hemolysis.

The Most Important Human Pathogen Streptococci and Enterococci

Streptococcus pyogenes (A Streptococci)
Pathogenicity factors:-
1. M protein:- has an antiphagocytic effect
2. Streptolysin O and streptolysin S:-Destroy the
membranes of erythrocytes and other cells
3. Pyrogenic streptococcal exotoxins (PSE) A,
B, C.:- Responsible for fever, scarlet fever
exanthem and enanthem, sepsis, and septic
shock.
4. Streptokinase:- Dissolves fibrin; facilitates
spread of streptococci in tissues.
5. Hyaluronidase:- Breaks down a substance
that cements tissues together.
6. Dnases:- Breakdown of DNA, producing
runny pus.

Streptococcus pneumoniae (Pneumococci)
• Pneumococci are Gram-positive, oval to lancet
shaped cocci that usually occur in pairs or short
chains.
• The cells are surrounded by a thick capsule.
Pathogenesis and clinical pictures:-
1. capsule:- protects the pathogens from
phagocytosis and is the most important
determinant of pneumococcal virulence.
2. Pneumolysin:- It has hemolysin effects on
membranes
• About 40–70% of healthy adults are carriers.
Pneumococcal infections usually arise from this
normal flora (endogenous infections).
• Predisposing factors include

– primary cardiopulmonary diseases,
– previous infections(e.g., influenza), and
– extirpation of the spleen or complement system
defects.

The most important pneumococcal infections are
lobar pneumonia and bronchopneumonia
acute exacerbation of chronic bronchitis
otitis media, sinusitis, meningitis, and corneal ulcer. Severe pneumococcal
infections frequently involve sepsis
Therapy:- Penicillin is the antibiotic of choice
Gram appearance and colony morphology of pneumococcal

 Streptococcus agalactiae (B Streptococci)
• B streptococci occasionally cause infections of the
skin and connective tissues, sepsis, urinary tract
infections, pneumonia, and peritonitis in
immunocompromised individuals.
• In the early onset form, the infection is caused intra
partum by B streptococci colonizing the vagina.
• Potential predisposing factors include birth
complications, premature birth, and a lack of
antibodies to the capsule In mother and neonate.
• Oral Streptococci:- Responsible for 50–70% of all
cases of bacterial endocarditis

• The origins of endocarditis lie in invasion of
the vascular system through lesions in the
oral mucosa.
• Responsible for dental caries

Gram Positive rods

1. Bacillus anthracis and anthrax
• Was the first bacterium shown to be the cause of a disease.
– In 1877, Robert Koch grew the organism in pure culture,
– Demonstrated its ability to form endospores,
– Produced experimental anthrax by injecting it into
animals.
Morphology of B. anthracis
– Gram-positive(young colony)
– nonmotile rods
– catalase and oxidase positive
– sporeforming rod
– can be cultivated in ordinary nutrient medium under
aerobic or anaerobic conditions.
Anthrax
• Anthrax is primarily a disease of domesticated and
wild animals
– herbivorous animals, such as cattle, sheep,
horses, mules, and goats.
• Humans become infected incidentally when
brought into contact with
– diseased animals, which includes their flesh,
bones, hides, hair and excrement.
• The most common form of the disease in humans
is cutaneous anthrax
 Cutaneous anthrax
• It is usually acquired via injured skin or mucous
membranes.
– The spores vegetative cells multiply
gelatinous edema develops at the sitepapule
within 12-36 hrs after infectionvesicle
malignant pustule necrotic ulcer
disseminate, giving rise to septicemia.
• Lymphatic swelling also occurs within seven days.
• In severe cases, where the blood stream is
eventually invaded, the disease is frequently fatal.
 Inhalation anthrax (woolsorters' disease)
• Results most commonly from inhalation of spore-
containing dust where animal hair or hides are being
handled.
• The disease begins abruptly with high fever and chest pain.
• It progresses rapidly to a systemic hemorrhagic pathology
and is often fatal if treatment cannot stop the invasive
aspect of the infection.
 Gastrointestinal anthrax
• Intestinal anthrax results from the ingestion of poorly
cooked meat from infected animals.
• GI anthrax is rare, but may occur as explosive outbreaks
associated with ingestion of infected animals.
• Intestinal anthrax has an extremely high mortality rate.
2. Clostridium
• Their natural habitat is the soil.

• Pathogenicity :- Production of exotoxins and/or
exoenzymes.
1. C. perfringens:- Causes of cellulitis and gas
gangrene (clostridial myonecrosis)
2. C. tetani:- Cause tetanus . This pathogen
produces the exotoxin tetanospasmin
3. C. botulinum :- Cause botulism a type of food
poisoning . These substances inhibit stimulus
transmission to the motor end plates.
4. C. difficile:- Cause pseudomembranous colitis and
it produces an enterotoxin (A) and a cytotoxin (B).
• Diagnosis of clostridial infections requires
identification of the pathogen (gas gangrene)
and/or the toxins (tetanus, botulism, colitis).
Treatment:- All clostridia are readily sensitive to
penicillin G.
• Antitoxins are used in therapy of tetanus and
botulism and hyperbaric O2 is used to treat gas
gangrene.
• The most important preventive measure against
tetanus is active vaccination with tetanus toxoid.
3. Corynebacterium
• There are five genera with Corynebacterium most
pathogenic
• Corynebacterium
Non spore formig, gram negative rods
 contain mycolic acid in the cell wall
 Form V, Y and club shaped polymorphic)
 colonize skin, URT, urogenital tract of
healthy people
 More than 60 species are known and few are
associated human disease.
C. diphtheriae
.  Club shaped
 Metachromic granules (energy storing) and
gives beaded appearance
 Join and form different angles (chine's letter)
 Based on colony morphology, biochemical
reactions, severity of disease, contain four
biovars:-
Gravis, mitis, intermedius, and belfanti
 Intermedius and belfantis are less virulent

Disease is totally due to effect of exotoxin
(absorption)
Exotoxin is encoded by the tox gen which is
introduced by lsyogenic bacteriophage

• Before secretion
a) The leader sequence should be proteolytically
cleaved
b) The toxin should be cleaved in to A and B poly
peptide
The toxin has three parts (A-B toxin)
1. Receptor binding region (B)
2. Translocation region (B)
3. Catalytic region on A

Respiratory diphtheria
Organism multiply, epithelial cells of pharynx,
tonsils or larynx( fever, sore throat , exudative
pharyngitis)
Psuedomembrane (exudative structure) will be
formed on pharynx which contain bacteria,
lymphocytes, plasma cells, fibrins, and dead cells)
Can cover tonsils, Uvula, palate or extend up to
nosopharynx or down to pharynx.
(breathing obstruction, damage of heart, coma and
death)
Don’t attempt to remove the membranebleeding
Cutaneous diphtheria
• Enter through broken skin
 Papule on skin which leads non healing ulcer
 Papule may be covered grayish membrane
Epidemiology
 World wide disease and common among people
living in crowded conditioned and non
immunized.
• Asymptomatic carriers maintain the bacteria in the
population
• Is pediatric disease but shifted to older age adults
in areas where there is active immunization( for
children).
4. Mycobacterium tuberculosis
Introduction
• Tuberculosis (TB) is a common and deadly infectious
disease
– Caused by Mycobacterium, mainly
Mycobacterium tuberculosis (MTB).
– M. bovis, M.africanum, M. canetti, and M. microti
can also cause tuberculosis
• Tuberculosis most commonly attacks the lungs
(Pulmonary TB)
• But can affect any parts of the body such as CNS, the
lymphatic system, the circulatory system, the
genitourinary system, bones, joints and even the
skin.
• Today, despite advances in treatment, TB is a global
pandemic
• It is fueled by the spread of HIV/AIDS, poverty, poor
health infrastructure and the emergence of drug-
resistant strains
• Indeed, the HIV/AIDS epidemic has produced a
devastating effect on TB control worldwide.
• 1/10 immunocompetent people infected with M.
tuberculosis will fall sick in their lifetimes
• Among those with HIV infection, one in ten per year
will develop active TB.
• In developing countries, the impact of HIV infection
on the TB situation, especially in the 20-35 age group,
is overwhelming.
The tubercle bacillus:
• Non-motile and non-sporulated rods
• They, have a high content (61-71 %) of G+C in
the genomic
• Have a high lipid content in the wall, probably
the highest among all bacteria.
• Several mycolic acids in the envelope structure
distinguish the mycobacteria
• Lipids constitute more than half of the dry
weight of the mycobacteria.

• The waxy coat confers the idiosyncratic
characteristics of the genus:
– acid fastness
– extreme hydrophobicity
– resistance to injury, including that of

many antibiotic

Figure. Structure of an
02/23/2021
Acid-Fast Cell Wall
Shimelis Teshome (BSc MLS) 37
Pathogenesis of MTB
• It is estimated about 90% of infected people with MTB
have asymptomatic
• Only 10% of LTBI will progress to active TB.
• TB infection begins when the mycobacterium reaches the
pulmonary alveoli, where they invade and replicate within
alveolar macrophages.
• Bacteria are picked up by DC, which do not allow
replication, and transport the bacilli to local lymph nodes.
– MTB further spreads through the bloodstream to the
more distant tissues and organs
– Secondary TB lesions can develop in lung apices,
peripheral lymph nodes, kidneys, brain, and bones
– All parts of the body can be affected by the disease
Clinical features
• TB in the lungs may cause symptoms such as

– a cough lasting three or more weeks that may
produce discolored or bloody sputum
– unintended weight loss
– fatigue, slight fever, night sweats, chills, loss
of appetite, and pain with breathing or
coughing
• Tuberculosis also can target almost any part of
the body, including joints, bones, urinary tract,
central nervous system, muscles, bone marrow
and lymphatic system.
Clinical features
• When TB occurs outside the lungs, signs and

symptoms vary, depending on the organs
involved for example:
– tuberculosis of the spine may result in back
pain, and tuberculosis
– that affects the kidneys might cause blood in
urine.
– Tuberculosis can also spread through the entire
body, simultaneously attacking many organ
systems.
Gram Negative Pathogenic bacteria


Helicobacter
•There are 22 species
•Three species are currently considered to be human pathogens
–Helicobacter pylori (human; no animal reservoir)
–H. cinaedi (male homosexuals; rodents)
–H. fenneliae (male homosexuals; rodents)
–In humans, enterohepatic helicobacters, such as H. canadensis,
H. canis, H. pullorum and H. winghamensis, have been isolated

• Enterohepatic helicobacters have been linked to
severe inflammatory lesions in the lower bowel,
gall bladders, and livers of infected humans
H. pylori
• Commonly associated with
Gastritis
peptic ulcers
gastric adenocarcinoma, lymphoma
• Highly motile (polar flagella)
• Young culture spiral shaped
• Old culture assume coccoid shape
• Produce abundance urease (isolate which colonize
stomach)
• Don't oxidize or ferment CHO
• The principal means of energy production and
biosynthesis is believed to occur via glycolysis and
gluconeogenesis
• Microaerophilic and need high CO2
 Pathogencity
• Virulent factors are responsible for
– Gastric inflammation
– Alteration of gastric acid production
– Tissue destruction

Initial colonization is facilitated by:-
A. Blockage of acid production (acid inhibitory
proteins)
B. Neutralization of gastric acid by ammonia
C. The bacteria penetrate (active motile) and pass
the gastric mucosa and adhere to epithelia cells
(Cork screw type motility)
D. Localized tissue damage will occur by urease,
mucinase, phospholipase, vacuolating cytotoxins
E. Produces catalase and superoxid dismutase
which prevents intracellular killing
Campylobacter
• Cause an acute gastrointestinal illness.
• Infection with this organism occur in every part
of the world.
• In developing countries, especially those in
tropical areas, they are hyperendemic
– Important causes of morbidity and mortality
in young children.
Morphology
• Small comma shaped gram negative rods
– Distinctive rapid darting motility (long
sheathed polar flagellum at one (polar) or
both (bipolar) ends of the cell)
Campylobacter……
– Microaerophilic & capnophilic
5%O2,10%CO2,85%N2
– Thermophilic (42-43C)
• There are 16 species which are associated with
human infections
• Campylobacter primarily cause G/E and
occasionally septicemia.
• Most G/ E is caused by C. jejuni followed by C.
coli.

Pathogenesis
Three factors important in the ability of
Campylobacter to produce illness include
– The dose of organisms reaching the small
intestine,
– The host’s immunity to the organism
– The virulence of the particular strain
• Some people infected with as few as 500
organisms while others need >106 CFU
– Sensitive to gastric acid
• Conditions which neutralize or decrease
gastric acid favor infections
• Guillain-Barre Syndrome (GBS)
Is an autoimmune condition, in which the
patients develop antibodies against
gangliosides, resulting in
– Axonal degeneration through demyelinization
• Carbohydrate mimicry between GM1 and
C. jejuni (O:19)
• LOS leading to the development of such
cross-reactive antibodies
– Reactive arthritis(immune related, swelling
joint)
C. fetus has capsule like proteins (S-protein)
which prevent form complement mediated
killing  septicemia
Symptoms
The enteric disease caused by C. jejuni or C. coli is
characterized
 profuse watery diarrhea (10 or more bowel
movement per day),
 fever, abdominal pain, nausea, and sometimes
bloody stools.
 Pain which sometimes mimic those of acute
appendicitis, is common features of
Campylobacter enteritis
Infection usually resolves spontaneously without
antimicrobial treatment.
Entrobacteriaceae(enteric
bacteria)
Enterobacteriaceae….
• Live in the intestinal tracts of animals in

health and disease.
• Gram-negative, oxidase-negative, rod-shaped,
motile by peritrichous flagella, facultative
anaerobes, ferment glucose producing acid and gas.
• Escherichia, Enterobacter, Klebsiella, Proteus,
Morganella, Providencia, Salmonella, Shigella and
Yersinia
• Enterobacteriaceae are distributed worldwide.
– They are found in water, soil , insects, fruits, vegetables,
grains, flowering plants, trees and as normal intestinal
flora in humans and many animals.
Enterobacteriaceae….
Human Pathogens
• Enterobacteriaceae are divided into pathogens and
nonpathogens based on their ability to cause
diarrheal disease of humans.
– The pathogenic genera were Salmonella, Shigella ,
E. coli and Yersinia
• E. coli causes at least five types of gastrointestinal
disease in humans.
– Pathogenicity in E. coli strains is due to the presence
of one or more virulence factors, including
• invasiveness factors (invasins),
• heat-labile and heat-stable enterotoxins, and
• colonization factors or adhesins.
Feces from humans or animals
containing pathogenic microbes or
their toxins
Food Fluid(milk or
water) Finger
Ingestion of
organism and/or
toxin
Gut
Organism multiply and toxin produced Organism invade or

but infection remains to localized in GIT toxin absorbed
Diarrhea Dissemination
Symptoms of systemic
Pathogen excreted in feces
infections
1. Escherichia coli Infections
E. coli is part of the normal flora of the colon in humans
and other animals
Can be pathogenic both within and outside of the GI
tract
The differences in the degree of virulence of different E.
coli strains are caused by
 The individual plasmid and
 Integrated prophage repertoire associated with each
strain
E. coli has fimbriae or pili that are frequently important
for adherence to host mucosal surfaces
Different strains of the organism may be motile or non
motile.
Clinical significance: intestinal disease
Transmission of intestinal disease is commonly by the
fecal/oral route
At least five types of intestinal infections that differ in
pathogenic mechanisms have been identified
Enterotoxigenic (ETEC)
enteropathogenic (EPEC)
enterohemorrhagic (EHEC)
enteroinvasive (EIEC) and
enteroaggregative (EAEC)
All are basically the same organism, differing only by
the acquisition of specific pathogenic traits
Clinical significance: extraintestinal
disease
• The source of infection for extraintestinal
disease is frequently the patient's own
flora
• in which the individual's own E. coli is
nonpathogenic in the intestine.
• However, it causes disease in that
individual when the organism is found in
the bladder or bloodstream (normally
sterile sites)
Urinary tract infections (UTI):
E. coli is the most common cause of UTI, including cystitis
and pyelonephritis.
Uncomplicated cystitis (the most commonly encountered
UTI) is caused by uropathogenic strains of E. coli
Characterized by
 P fimbriae (an adherence factor)
 hemolysin,
 colicin V and
 Resistance to the bactericidal activity of serum
complement.
Complicated UTI (pyelonephritis) occurs in settings of
obstructed urinary flow, which may be caused by
nonuropathogenic strains
Neonatal meningitis:
• E. coli is a major cause of this disease occurring within
the first month of life.
• The K1 (capsular) antigen is particularly associated
with such infections.
The most common causes of neonatal meningitis:
• Group B streptococcus, E. coli and Listeria
• The most common causes of neonatal sepsis with
or without meningitis: Group B streptococcus and
E. coli
Nosocomial (hospital-acquired) infections:
These include sepsis/bacteremia, endotoxic shock, and
pneumonia.
2. Salmonella
• Salmonella adopted in honor of Dr. Salmon, who
discovered Salmonella from infected pig in 1885.
• Contaminated animal products
• Salmonellosis - mild
• Typhoid fever – severe
• Normal flora in animals
• A major health problem
Non-typhoidal salmonellosis
– Mainly due to S. Enteritidis, S. Typhimurium
– 1.3 billion cases and 3 million deaths/y
Salmonella
 Typhoid fever/Enteric fever
– Mainly due to S. Typhi
– >21 million cases and 700,000 deaths/y
 Salmonella:-
Gram negative, facultative anaerobes bacilli, Glucose
fermenters, oxidase –ve, motile (most), non capsulated
except, S. Typhi, S. Paratyphi C and S. Dublin.
 Antigens
A. O (somatic antigen) used for Serogrouping
Represented by letters or numbers
B. H (flagellar) antigen
C. Vi antigens
Found in S. Typhi, S. Paratyphi and some strains of S.
Dublin.
Clinical disease
Salmonella infection results:-
a. Gastroenteritis
b. Septicemia/ systemic infection
c. Enteric fever
d. Asymptomatic colonization
 G/E
Symptoms appear after 6 to 48 hrs
Nausea, vomiting, non-bloody diarrhea, fever,
abdominal crump, myalgias and head ache

 Septicemia
 Can be caused by all serotype, commonly caused
by
S. Choleraesuis, S. Paratyphi, S. Typhi
 Common in children, geriatric patient and in
immuno-compromized patient
 Enteric fever
 Caused by:- A. S. Typhi_ typhoid fever
B. S. paratypi A, B, C- paratypoid (mild
typhoid)
 Bacilli pass lining of SIengulfed by macrophage
 bld  liver, spleen, bone marrow, replicate 
gall bladder and SI  perforation and hemorrhage
3. Shigella
• Discovered by Japan microbiologist Shiga 100
years ago
• The genus consists of four species( biochemical,
serology) : S. dysentriae, S. flexneri , S. bpydii, S.
sonnei
• All Cause Shigellosis or bacillary dysentery
• Shigella dysenteriae: causes most serious form of
bacillary dysentery
• Shigella flexneri: most common cause of shigellosis
in underdeveloped countries
• Shigella sonnei: most common cause of shigellosis
in developed countries
Clinical features
Incubation time is 1 to 3 days
Characterized by:-
Abdominal crump, diarrhea, fever
Pus and blood in stool (due to colonic invasion)
Epidemiology
Human is the only host
Transmitted by feco-oral route
Shigellosis is common in communities with low
sanitation and personal hygiene

• 200 bacilli can initiate the disease (contagious)
• Epidemic is common in closed communities like,
daycare centers, nurseries, etc.
 Treatment
Guided by susceptibility tests
Empirical therapy can be initiated with
fluroquinolones or SxT(cotrimoxazole,
trimethoprim-sulfamethoxazole)
 Prevention
1. Sanitary control of food and water/personal hygiene
2. Detection of carriers particularly in food handlers
3. Rx of infected individuals
Pseudomonas aeruginosa
Morphology: Gram stain of P.
aeruginosa
 Gram-negative rod
 Motile (single
polar Flagellum)
 Some are
encapsulated
 Non fermenative
Pseudomonas aeruginosa……
 Pathogenesis
It is an opportunistic pathogen
 Need some breach in Io host defense to
initiate an infection
P. aeruginosa has many virulence factors
1. Structural components
2. Toxins
3. enzymes
Vibrio cholera
•Genus Vibrio contains 60 species

•Primarily found in water and cause G/E
•10 species are related to human infections
•V. cholera, V. parahaemolyticus, C.
vulnificus are medically important
General characteristics
Gram negative curved rods, motile (polar
flagella), oxidase positive,
 Grow B/n 14-40oC, most are halophilic
 Grow best at alkaline pH

Vibrio cholera…….
• Individuals with low HCL are susceptible

• Found in fresh and marine water and
associated with aquatic animals.
• Posses polar flagella, pili
• O polysaccharide in LPS used for

serogrouping
• Has over 140 identified serotypes based on O-
antigen(O1-O139)
• Only O1 and O139 are toxigenic(produce cholera
toxin) and cause epidemic Cholera disease
• Vibrio O1 divided into
3 serotypes:-Inaba, Ogawa, Hikojima
Virulence factors (O1, O139)
Cholera toxin:- Hyper secretion of electrolyte and water
 A-B type of toxin
 Encoded on a filamentous phage (ctxΦ) that is capable
of transducing the ctx gene into other cholera strains
Pili:- adherence to intestinal cells and binding site for
phages
Neuraminidase:- cleaves sialic acid from some cell
that can be used as receptor for pili

N. Gonorrhoeae (gonococcus)
N. Gonorrhoeae….
 Morphology and physiology

Aerobic Gram-negative diplococci, non spore former,
non motile, oxidase and catalase positive, usually seen
in pairs with adjacent flattened sides
Frequently found intracellularly in polymorphonuclear
leukocytes
Fimbriae, which play a major role in adherence, extend
several micrometers from the cell surface

N. Gonorrhoeae….
• Possesses a typical Gram-negative outer membrane

composed of proteins, phospholipids, and
lipopolysaccharide (LPS).
• Distinguished from enteric LPS by its
– Highly-branched basal oligosaccharide structure
– The absence of repeating O-antigen subunits.
– Thus neisserial LPS is referred to as lipooligosaccharide
(LOS).
• The bacterium characteristically releases outer
membrane fragments called "blebs" during growth.
– Blebs contain LOS and probably have a role in pathogenesis
if they are disseminated

N. Gonorrhoeae….
Infections caused by N. gonorrhoeae
• Gonorrheal infection is generally limited to
superficial mucosal surfaces lined with
columnar epithelium.
– The areas most frequently involved are the
urethra, cervix, rectum, pharynx, and
conjunctiva.
• Mucosal infections are usually characterized
by a purulent discharge.
• Uncomplicated gonorrhea symptom in the adult
male is
– a discharge that may range from a scanty, clear or
cloudy fluid to one that is copious and purulent.
– Dysuria and intense burning and pain upon urination.
– Inflammation of the urethral tissues results in the
characteristic redness, swelling, heat, and pain in the
region.
• Endocervical infection is the most common form of
uncomplicated gonorrhea in women.
• Usually characterized by
• vaginal discharge and sometimes by dysuria.
• About 50% of women with cervical infections are
asymptomatic.
N. Gonorrhoeae….
– In the male, the organism may invade the

prostate resulting in prostatitis, or extend
to the testicles resulting in orchitis.
• In the female, cervical involvement may
extend through the
– uterus to the fallopian tubes resulting in
salpingitis, or to the ovaries resulting in
ovaritis.
• The involvement of testicles, fallopian tubes
or ovaries may result in sterility.
N. Gonorrhoeae….
• Rectal infections with N. gonorrhoeae occur in
about one-third of women with cervical infection.
• They most often result from autoinoculation with
cervical discharge and are rarely symptomatic.
• Ocular infections by N. gonorrhoeae can have
serious consequences of corneal scarring or
perforation.
• Ocular infections (ophthalmia neonatorum) occur
most commonly in newborns who are exposed to
infected secretions in the birth canal .
N. meningitidis(meningococci)
• N. meningitidis posses capsules which is used for
serogroupings.
– There are12 serogroups (A, B, C, H, I, K, L,
W-135, X, Y,Z, 29E)
– Different serogroup responsible disease in
different areas
– Group A is common in Africa, Group C and A
are associated with epidemic disease
– Proteins and antigens in LOS used for
serotyping
Haemophilus
• Pasteurellaceae has three genera
Haemophilus
 Actinobacillus
Pasteurella
Haemophilus (blood loving)
gram-ve, short rods, pleomorphic bacteria
Spcies
H. influnzae- more pathogenic
H. aegyptius- acute purulent conjunctivitis
 H. influnzae
• It is a free-living, humanadapted organism without another
reservoir
• Its principal habitat is the nasopharynx, but it is found inhabiting
other mucosal surfaces including the genital tract and occasionally
the intestinal tract
some strains are capsulated
a. Serotypes a to f ( based on capsular antigens)
Hib is most virulent
b. biotypes I to VIII( biochemical)
 Encapsulated, Hib(biotype I) most pathogenic
 May present in small no. in URT of healthy people
 Cause meningitis , epiglottitis, cellulites (unvaccinated child)
Chlamydiae
Definition and classification
• Small, obligate cell parasites with a Gram-negative cell
wall.
• The reproductive cycle of the chlamydiae comprises two
developmental stages:
– The elementary bodies are optimally adapted to survival
outside of host cells.
– Reticulate bodies, are the form in which the chlamydiae
reproduce inside the host cells by means of transverse fission.

• Three human pathogen species of chlamydiae are
known:
– C. psittaci
– C. trachomatis (with the biovars trachoma and
lymphogranulomavenereum), and
– C. pneumoniae.

C. trachomatis
is a pathogen that infects only humans

Bordetella
• Extremely small aerobic gram negative cocco bacilli
• Contain seven species and 3 are associated with human
disease
• B. pertussis- whooping cough
• B. paraprtusis- Mild form of pertussis
• B. bronchiseptica- 10 disease of animal may cause
bronchopneumonia
• Species classification is based
1. Growth characteristic
2. Biochemical reaction
3. Antigenic properties

B. pertussis
• Colonize respiratory epithelium
• Gram negative aerobic coccobacillus
• Oxidize only aas not CHO
• Virulent factors
a. attachment proteins
1.Pertactin(P69) and filamentous hemagglutinis
Has receptors on membranes of ciliated respiratory cells
Binds on CR3( glycoprotien receptor on macrophage)

7.systemic Bacteriology

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7.systemic Bacteriology

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Systemic bacteriology

Shimelis Teshome (BSc MLS)

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B. Culture on blood agar: small,

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• Predisposing factors include

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• Their natural habitat is the soil.

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– resistance to injury, including that of

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• TB in the lungs may cause symptoms such as

• When TB occurs outside the lungs, signs and

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• Live in the intestinal tracts of animals in

Organism multiply and toxin produced Organism invade or

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•Genus Vibrio contains 60 species

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• Individuals with low HCL are susceptible

• O polysaccharide in LPS used for

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 Morphology and physiology

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• Possesses a typical Gram-negative outer membrane

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– In the male, the organism may invade the

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