GRAM NEGATIVE COCCI & GRAM

NEGATIVE BACILLI

STEVEN, ALAFI,DICKSON,ANGE,JOEL
GRAM NEGATIVE COCCI BACTERIA
1. NEISSERIA MENINGITIDIS
(Meningococcus)
 Introduction
● Meningococci are Gram-negative cocci bacteria.
● Meningococci are strict human parasites
inhabiting the nasopharynx.
● In some, local inflammation ensues with rhinitis
and pharyngitis.
● Dissemination occurs only in a small proportion.
 Introduction - Morphology
● They are oval or spherical in shape (0.6-0.8 μm in
size).They are typically arranged in pairs, with the
adjacent sides flattened or concave opposing
edges and the long axes parallel.
● They are typically seen in large numbers inside
polymorphonuclear leukocytes.
● Considerable variations occur in size, shape and
staining properties, especially in older cultures,
due to autolysis.
 Introduction - Cultural characteristics
● Most fresh isolates are encapsulated.
● They are non sporing and nonmotile.
● Meningococci have exacting growth
requirements and do not grow on ordinary media.
● Growth occurs on media enriched with blood,
serum, or ascitic fluid, which promote growth
rather than providing additional nutritional needs
by neutralizing certain inhibiting substances in
culture media.
 Introduction - Cultural characteristics
● Strains grows on Mueller-Hinton medium
without the addition of blood or serum but grow
poorly if at all on most unenriched media.
● They are strict aerobes, no growth occurring
anaerobically.
● The optimum temperature for growth is 35-36°C.
 Epidemiology
● Humans are the only natural carriers for N.
meningitidis.
● Studies of the asymptomatic carriage of N.
meningitidis have shown that there is a
tremendous variation in its prevalence, from less
than 1 percent to almost 40 percent.
 Epidemiology cont’d
● The oral and nasopharyngeal carriage rates are
highest for school-aged children and young
adults are higher in lower socioeconomic
populations (caused by person-to-person spread
in crowded areas).
● The carriage rates do not vary with the seasons
even though disease is most common during the
dry, cold months of the year.
 Epidemiology cont’d
● An increase in carrier rate heralds the onset of an
epidemic. The carrier state may last for a few days
to months.
● The carrier rate is higher in the members of the
household of a patient with meningococcal
disease.
● Household contacts of a case are 500-800 times
more likely to develop meningococcal infection
 Epidemiology cont’d
● During epidemics, the carrier rates in closed
communities may go up to 90 percent.
● Endemic disease is most common in children
younger than 5 years, particularly infants.
● People who are older and who live in closed
populations are prone to infection during
epidemics.
 Pathophysiology

The majority of cases of meningitis are caused by

an infectious agent that has colonized or established
a localized infection in the host.
An infectious agent can gain access to the CNS and
cause meningeal disease via any of the three
following major pathways:
Pathophysiology

● Invasion of the bloodstream and subsequent

hematogenous seeding of the CNS
● A retrograde neuronal (eg, olfactory and
peripheral nerves) pathway
● Direct contiguous spread
 Pathophysiology
Meningococcal, cryptococcal, syphilitic, and
pneumococcal meningitis all use bloodstream
invasion. Septic thrombi or osteomyelitic erosion
from infected contiguous structures are rare causes
of meningitis. Meningeal seeding can also occur
with a direct bacterial inoculate during trauma,
neurosurgery, or instrumentation.
 Pathophysiology
Possible pathways for the migration of pathogens
from the middle ear to the meninges include the
following:
● The bloodstream
● Preformed tissue planes (eg, posterior fossa)
● Temporal bone fractures
● The oval or round window membranes of the
labyrinths
 Pathophysiology

The meninges form a natural barrier between the

bloodstream and the brain, protecting it from the
body's immune system. This protection is normally
advantageous because it prevents the immune
system from attacking the brain.
 Pathophysiology

The blood-brain barrier, however, can be disrupted

in meningitis; once bacteria or other organisms have
made their way to the brain, they are somewhat
isolated from the immune system and can spread.
 Pathophysiology

When the body attempts to fight the infection, blood

vessels leak, allowing fluid, WBCs, and other
infection-fighting particles to enter the meninges
and brain. This process, in turn, causes brain
swelling and can eventually result in decreased
blood flow to parts of the brain, exacerbating
infection symptoms.
 Pathophysiology
The inflammatory process may remain confined to
the subarachnoid space depending on the severity of
bacterial meningitis. The pial barrier is not
penetrated in less severe forms, and the underlying
parenchyma remains intact. However, in more severe
cases of bacterial meningitis, the pial barrier is
breached, and the inflammatory process invades the
 Pathophysiology

As a result, bacterial meningitis can cause

widespread cortical destruction, especially if left
untreated. Bacterial replication, an increase in
inflammatory cells, cytokine-induced disruptions in
membrane transport, and increased vascular and
membrane permeability all contribute to the
infectious process in bacterial meningitis.
 Pathophysiology
These processes are responsible for the distinctive
changes in CSF cell count, pH, lactate, protein, and
glucose found in patients with this disease.
 Pathophysiology
Exudates spread throughout the CSF, especially to
the basal cisterns, causing the following:
● Damage to cranial nerves (eg, cranial nerve
VIII, with resultant hearing loss)
● Obliteration of CSF pathways (causing
obstructive hydrocephalus)
● Induction of vasculitis and thrombophlebitis
(causing local brain ischemia)
 Pathophysiology

Cerebral Edema: Interstitial edema is caused by

increased CSF viscosity caused by plasma
component influx into the subarachnoid space and
decreased venous outflow. Cytotoxic edema is
caused by the accumulation of bacterial degradation
products, neutrophils, and other cellular activation.
 Pathophysiology

Cytokines and secondary mediators in bacterial

meningitis: Patients with bacterial meningitis have
elevated CSF concentrations of TNF-, IL-1, IL-6,
and IL-8. Cytokine levels, including IL-6, TNF-,
and interferon gamma, are elevated in aseptic
meningitis patients.
 Pathophysiology

Cerebral fluid and intracranial pressure:

Increased intracranial pressure is one of the
complications of meningitis (ICP). Interstitial
edema and cytotoxic edema caused by the release of
toxic factors from bacteria and neutrophils, and
vasogenic edema (increased blood brain barrier
permeability) are all thought to play a role.
 Diagnosis
Specimens
i. Cerebrospinal fluid (CSF).
ii. Blood for culture (which may come from a
patient with meningitis, a hemorrhagic rash or
pyrexia of uncertain origin).
iii. Aspirate from skin lesions or pus from an
infected joint.
iv. Throat or nasopharyngeal swabs from suspected
cases.
 Diagnosis cont’d
● Swabs should be transported in Stuart’s transport
medium.
● All specimens where meningococcal infection is
suspected must be submitted to the laboratory
immediately.
1. Examination of CSF
2. Blood Cultures
 Diagnosis cont’d
3. Petechial lesions: Meningococci may sometimes
be demonstrated in petechial lesions by microscopy
and culture
4. Serological diagnosis: Paired sera may be tested
for the presence of complement-fixing antibodies.
This test is helpful in cases where no organisms
have been isolated or in obscure pyrexias, which
may be due to chronic meningococcal septicemia.
 Diagnosis cont’d
5. Pus, aspirates and swabs: Gram-stained films
are examined. In addition to blood agar and
chocolate agar, Thayer-Martin selective medium is
used for the culture of materials expected to yield a
mixture of organisms such as pus, aspirates, and
throat, nasopharyngeal and genital swabs.
 Diagnosis cont’d
6. Polymerase chain reaction: Group specific
diagnosis of infection can be made by detection of
meningococcal DNA sequence in CSF or blood by
PCR amplification.
 Treatment
● Penicillin is currently the antibiotic of choice, but
resistance to it is also becoming more common.
Intravenous penicillin G is the treatment of choice.
● Chloramphenicol is effective, but risks of blood
dyscrasia have limited its use. Either
chloramphenicol or a third generation
cephalosporins such as cefotaxime or ceftriaxone
is used in persons allergic to penicillin allergy.
 Treatment
● Penicillin is currently the antibiotic of choice, but
resistance to it is also becoming more common.
Intravenous penicillin G is the treatment of choice.
● Chloramphenicol is effective, but risks of blood
dyscrasia have limited its use.
● Either chloramphenicol or a third generation
cephalosporins such as cefotaxime or ceftriaxone
is used in persons allergic to penicillin allergy.
 Treatment
● At the end of a course of therapy with penicillin, it
is important to give eradicative treatment with
rifampicin or ciprofloxacin because penicillin does
not eradicate meningococci from the nasopharynx
and a patient returning home as a carrier may
infect others.
● This probably does not apply to ceftriaxone or
cefotaxime.
 Control ( Prophylaxis)
Chemoprophylaxis
➢ Sulphonamides were used for prophylaxis, but
are not effective due to resistance. In addition,
penicillin is effective in eliminating the carrier
state.
➢ Minocycline and rifampin have been used
effectively for antibiotic mediated
chemoprophylaxis.
 Control (Prophylaxis)
➢ Ciprofloxacin is widely used as a prophylactic for
adolescents and adults as a single, oral dose.
➢ All household and other intimate contacts of a
case should be given chemoprophylaxis as a
routine.
Immunoprophylaxis
● A polyvalent vaccine effective against serogroups
A, C, Y, and W135, which can be administered to
children older than 2 years, has been developed.
2. Neisseria Gonorrhoeae
 Introduction
● N. gonorrhoeae are Gram-negative and aerobic
diplococci.
● It is the causative agent of gonorrhea, one of the
most common sexually transmitted disease
worldwide.
● Gonococci when transmitted nonsexually from
the mother’s genital tract to the newborn during
birth cause ophthalmia neonatorum.
 Introduction
● Freshly isolated bacteria may be encapsulated.
● They do not form endospores.
● They are nonmotile.
● They are aerobes but can also grow anaerobically.
● N. gonorrhoeae is a fastidious coccus.
● It requires complex media for growth.
● The cocci grow on enriched media, such as blood
or chocolate agar.
 Epidemiology
Geographical Location
Gonococcal infection has been reported all over the
world. However, the incidence is much lower in
European countries, and Sweden has virtually
eliminated this condition. In developing countries,
gonorrhea and its complications are most common.
The estimated prevalence of gonorrhea in pregnant
women in Asia is 4%, 5% in Latin America, and
10% in Africa.
 Epidemiology
Habitat
N. gonorrhoeae is an exclusively human pathogen.
The gonococci can only be found in infected
environments. The gonococci are most commonly
found in the endocervix of infected women, and in
the urethra of infected men. Gonococci can be found
in both men and women's pharynx, rectum, and eyes.
 Epidemiology
Reservoir, source, and transmission of infection
Only humans, especially asymptomatic infected men
and women, are reservoirs of infections.
Asymptomatic carriage is more common in women
than in men. Purulent urethra or cervical discharge is
the most common source of infection.
 Epidemiology
The infection is transmitted:
■ Primarily by sexual contact. N. gonorrhoeae
infection occurs following mucosal inoculation
during vaginal, anal, or oral sexual contact.
Increased sexual contact with infected partners
increases the risk of acquiring the infection.
■ Less frequently, by nonsexual contact.
Ophthalmia neonatorum is acquired nonsexually.
 Epidemiology
This infection occurs following a conjunctival
inoculation during vaginal delivery. Less frequently,
the disease is transmitted through rectum,
oropharynx, or through the birth canal. Fomites do
not play any role in transmission of the disease,
because gonococci die rapidly outside the human
body.
 Pathophysiology
N. gonorrhoeae causes disease by first attaching to
mucosal cells. They then enter the cells, multiply
within them, and pass through the cells into the
subepithelial space, establishing the infection. Pili
aid in the attachment of gonococci to mucosal
surfaces and also contribute to resistance by
preventing PMN leukocyte ingestion and killing.
 Pathophysiology
The outer membrane proteins, such Opa proteins,
facilitate adherence between gonococci and also
increase adherence to phagocytes. The Opa proteins
also aid in the migration of gonococci into epithelial
cells. Por proteins prevent phagolysosome fusion in
phagocytes, shielding phagocytosed bacteria from
intracellular killing. The bacteria's production of
beta-lactamase (penicillinase) also contributes to the
invasion.
 Pathophysiology
The host response is characterized by leukocyte
infiltration, epithelial sloughing, the formation of
microabscesses in the submucosa, and the
production of purulent pus. The LOS of the
gonococcal cell wall stimulates the production of
tumor necrosis factor alpha (TNF-) and other
inflammatory responses, which contribute to the
majority of gonococcal infection symptoms.
 Diagnosis

Laboratory diagnosis of gonococcal infection

depends on demonstration of N. gonorrhoeae at the
site of infection.
Specimens: The genital (urethral discharge, cervical
discharge, etc.), rectal, and pharyngeal specimens
are collected for the isolation and identification of
gonococci.
 Diagnosis
Microscopy: Gram stain of urethral exudates: The
presence of four or more polymorphonuclear (PMN)
leukocytes per oil-immersion field in Gram-stained
urethral exudate smear is diagnostic of urethritis:
● Demonstration of typical Gram-negative
intracellular diplococci is characteristic of N.
gonorrhoeae (Fig. 26-3, Color Photo 22).
● Gram stain helps in the presumptive diagnosis of
the gonococcal infection.
 Diagnosis
It is more than 90% sensitive and 98% specific for
the diagnosis of gonococcal infection in
symptomatic males. However, in asymptomatic
males, the sensitivity of the Gram stain is only 60%
or less.
Cultures: Culture confirms the diagnosis of
gonorrhea by isolating N. gonorrhoeae from clinical
specimens.
 Diagnosis

Serodiagnosis: Serological tests are performed to

detect gonococcal antigens or specific anti-
gonococcal antibodies in the serum in order to
diagnose gonorrhea. ELISA and RIA
(radioimmunoassays) using whole cell lysates, pilus
proteins, and gonococci LPS antigens show
antibodies in the serum.
 Diagnosis
These serological tests should not be used on a
regular basis. These are only used in specific
circumstances, such as chronic gonorrhea,
gonococcal arthritis, and so on.
Diagnosis - Identification of N. Gonorrhoeae
 Treatment
Sulfonamides were used for treatment of gonorrhea.
In the beginning, all the strains of gonococci were
sensitive to sulfonamides but subsequently, they
developed resistance to these antibiotics.
Penicillin is the drug of choice for penicillin-
sensitive strains of N. gonorrhoeae however there
are penicillin-resistant strains of N. gonorrhoeae.
 Treatment
Alternative drugs in cases of penicillin resistance or
in penicillin-allergic individuals: Ceftriaxone,
cefixime, ciprofloxacin, or ofloxacin are the
alternative drugs in cases of penicillin resistance or in
penicillin-allergic individuals.
A single-dose regimen of any of these antibiotics is
given as an initial therapy in uncomplicated
urethritis, cervicitis, or rectal or pharyngeal
infections in adults.
 Treatment

Resistance to other antibiotics: Chromosomal-

mediated resistance to other antibiotics, such as
tetracycline, erythromycin, and aminoglycosides,
has also been reported.
 Prevention and Control (Prophylaxis)
Currently, there is no effective vaccine available
against N. gonorrhoeae. Chemoprophylaxis by the
prophylactic use of penicillin is also ineffective and
may promote the development of resistant strains.
Therefore, health education, early detection of cases,
tracing of contacts, and follow-up of screening of
sexual contacts is important in the prevention of
gonorrheal epidemics.
 Prevention and Control
Furthermore, the prevention of gonorrhea involves
the promotion of safe sex and individual
counseling. Gonococcal conjunctivitis in the
newborns is prevented by using erythromycin
ointment.
 3. Moraxella
Moraxella catarrhalis is a gram-negative, aerobic,
oxidase-positive diplococcus that belongs to the
genus Moraxella's subgenus Branhamella. It is now
thought to be a saprophyte of the upper respiratory
system with no apparent pathogenic implications.
The culture of Moraxella is used to confirm the
diagnosis of its infection, and the relevant diagnostic
techniques are chosen based on the site of infection
and the underlying illness.
 Culture characteristics
On Chocolate agar Moraxella appear;
● Pinkish brown
● Resemble N.gonorrhoeae

On Blood agar
● Small(less than 1mm)
● They pit the agar
● Some strains are hemolytic
● Grey/brown , smooth, round and uniform
 Epidemiology
Moraxella infections (M.catarrhalis) are more
common in children, but they can occur at any age.
Only a small fraction of positive cultures in the
pediatric population are pathogenic or noteworthy. A
study reported that 9% of cultures positive for
M.catarrhalis were discovered in children under the
age of five, and 33% in children aged six to ten.
However, all Moraxella species culture positive,
primarily M.catarrhalis, showed clinical significance
 Epidemiology
In children, M catarrhalis is the third most
prevalent cause of otitis media and sinusitis
(after Streptococcus pneumoniae and
Haemophilus influenzae). M catarrhalis is
thought to cause 3-4 million instances of otitis
media each year, with a $2 billion yearly
health-care cost (direct and indirect).
 Pathophysiology

Moraxella species, primarily M.catarrhalis,

invade primarily the upper respiratory tract,
Furthermore, it is transmitted through
direct contact with contaminated
individuals or through droplet secretions.
 Pathophysiology
M.Catarrhalis, a Moraxella species, produces a
lipopolysaccharide endotoxin identical to that seen
in Neisseria species and has a role in disease
pathogenesis. Because of their pili or fimbriae,
strains of the Moraxella species have a high
likelihood of adhering to the respiratory epithelium.
Furthermore, it contains proteins that aid in iron
uptake and resistance by interfering with the
formation of the membrane attack complex.
 Pathophysiology
Cold shock (26°C for 3 hours) has been demonstrated
to promote cell adhesion and proinflammatory
responses in M catarrhalis. This can happen
physiologically with extended exposure to cold air
temperatures, resulting in cold-like symptoms. In
both children and adults, Moraxella is a common
cause of otitis media, sinusitis, bronchitis, and
pneumonia. Immune responses to M catarrhalis
appear to be age-dependent, with immunoglobulin G
(IgG) titers steadily increasing in children.
 Diagnosis(Biochemical tests)
Oxidase test
● Moraxella species are positive for the oxidase
enzyme. However, Neisseria may be mistakenly
identified as moraxella species since its also
positive.
Tributyrin test
● This is 2-4hr presumptive test, M.Catarrhalis is
tributyrin positive which differentiates from
Neisseria species which are negative.
 Diagnosis(Biochemical tests)
DNase test
● This test differentiates the M.Catarrhalis from
other Moraxella species because it is positive for
the supplementary test.

Treatment
● Penicillin
● Amoxicillin
● Ampicillin
 Treatment and control
● M.catarrhalis has been shown to be resistant against
amoxicillin however, drugs such as ofloxacin are
effective on M.catarrhalis

CONTROL
● Hand washing
● Sterilization of aspiration tubes to avoid
nosocomial infections
● Good general health habits and Moraxella vaccine.
GRAM NEGATIVE BACILLI
1. Corynebacterium diphtheria
The typical club-shaped Corynebacterium
diphtheria is an anaerobic, gram-positive, non-
motile, non-spore-forming, non-capsulated,
pleomorphic coccobacilli that produces toxins. It
has four biotypes, namely gravis, mitis,
intermedius, and belfanti, based on biochemical
characteristics and colony shape.
The mild form of the disease is caused by C.
mitis, the intermediate type by C.
intermedius, and the severe form by C.
gravis. Risk factors for susceptibility and
infection transmission include poor living
conditions, a low socioeconomic status,
immunocompromised states, and insufficient
immunization.
T
Epidemiology
Corynebacterium diphtheriae can be
transmitted through direct contact, secretions,
or droplets. It has been shown that
nontoxigenic bacteria can undergo in situ
lysogenic conversion to a toxigenic
phenotype. The infection only spreads among
humans despite toxic strains being discovered
in horses.
In areas with ongoing vaccination campaigns,
isolated illness outbreaks are frequently
linked to a carrier recently traveling to a
subtropical area where diphtheria is
prevalent. In populations with inactive
immunization programs, large-scale disease
outbreaks may develop.
Pathophysiology
Respiratory droplets or contact transmission
from an infected host or their carrier are the
two modes of transmission. Direct interaction
with items or secretions that have previously
come into contact with the sick individual or
its carrier can also spread the disease. The
bacteria often populate the upper respiratory
tract after entering the host.
Typically, they don't enter tissue to produce
widespread bacteremia.
However, the toxigenic strains of these
bacteria create toxins, which are then released
into the blood and cause various clinical
symptoms. Endosome release of exotoxin
results in a localized inflammatory response,
followed by necrosis and tissue apoptosis.
Two proteins are linked to form the toxin.
NAD is catalytically transferred from NAD to
diphthamide by diphtheria toxin (DT), which
inactivates the elongation factor, blocking
protein synthesis and ultimately leading to
cell death. Local tissue must be destroyed for
the toxin to go to other body areas via blood
and lymph. The myocardium, kidneys, and
nervous system may be impacted by
developing diphtheria toxin.
Diagnosis
Combination of clinical manifestations of
nasopharyngeal diphtheria and a culture-
proven toxigenic C diphtheria infection of the
skin, nose, or throat is required for a clinical
diagnosis (e.g., sore throat, dysphagia, bloody
nasal discharge, pseudomembrane).
Numerous in vitro (such as gel
immunodiffusion and tissue culture) and in
vivo (such as rabbit skin test and guinea pig
challenge) techniques are used to determine
toxicity. After the antibiotics have finished
working, a nasopharyngeal and throat culture
should be performed.
Treatment
The cornerstone of treatment is the prompt
injection of diphtheria antitoxin combined with
antibiotic coverage. To reduce the number of
potential contacts, isolate every case and take
appropriate safety measures. As a result, it
works to neutralize diphtheria toxin in
circulation rather than poison attached to cells.
Because of this, it is empirical to deliver
antitoxin quickly following the creation of the
presumptive diagnosis, even before its
microbiological confirmation.
Antibiotics are given to patients to eradicate
harmful microorganisms. Penicillin and
erythromycin are the most often prescribed
antibiotics, typically used for at least two
Control
Diphtheria immunization starts early in infancy.
Beginning with the first dose in the series, which
is typically administered in the second month of
life, three initial doses are administered 4 to 8
weeks apart. The third dosage is followed by the
fourth dose, which is administered about a year
following the final primary vaccine.
2. Bacillus anthracis
Bacillus anthracite is a gram positive rod like
shaped bacteria that causes Anthrax.
It is an aerobic spore bearing bacillus.
Its name is derived from the Greek word that
means coal, B anthrakis.
This is because of its ability to cause a black,
coal-like cutaneous eschars.
B. anthracis: capsulated organism, pxo2 -
capsule Gene.
B. anthracis: capsulated organism, pxo2 -
capsule Gene.
The non-capsulated one is not virulent and it
does not induce anthrax.
Epidemiology
Bacillus anthracis causes anthrax which is a
worldwide zoonotic disease. It affects mostly
grazing herbivores. Human infections
especially cutaneous infections happens
through contact with animals that are infected
or through animal products that are
contaminated for example hides or wools.
Cases about inhalation occur through gases
from factories that deals with processing of
hides and wool. Pathogenicity of anthrax
spore through respiratory route is not high.
Lincoln and his team has given us a quote
that the spore load figure for sheep is very
susceptible to anthrax, that is 200000.
This study regards humans as being
moderately resistant to anthrax. The study of
Dahlgren and his team used the sample of air
techniques to estimate that in one woolen
mill, people take in 600 and 1300 spores in
an eight hour shift without any effect of
illness.
The largest human epidemic is shown in
Zimbabwe with a case of 10000 humans
which are mostly cutaneous in the year 1979
and 1985. From this epidemic three main
things were considered; 1. Vaccination of
animals on regular basis, 2. Human can
acquire it through a direct contact with
infected animals,
3. The risk of infection is very little in regards
to cross infections from infected patients to
health care workers.
EPIDEMIOLOGY
 Pathophysiology
ANTHRAX
It is the disease that basically affect herbivores.
The infection of human comes in three ways
1. Cutaneous or inoculation which is the most
common ( 1-7 days)
- there is a small papule at site of infection and
development of a ring of vesicles, coalesce.
- Erythematous ring: this is a small dark area at the
- Depressed - a black necrotic area that is at
the center ( black Eschar or a malignant
pustule).
- Lesions that is painless, it has no pus
unless if it is a secondary infection.
- Healing: it takes 1-2 weeks- there’s a
granulation dislodge and leaving a scar.
- Complications: sepsis (meningitis)
Pathophysiology
Anthrax
2.inhalation or woolsorter's Disease
- the incubation period is 6 weeks
- Mediastinal lymph nodes
- There’s a marked hemorrhagic necrosis
edema at the mediastinum
- There’s a pronounced widening of the
mediastinum
 Pathophysiology cont
- There’s a respiratory infection viral mimic. It is
rapidly progressive and a severe infection of the
pulmonary system.
- COMPLICATIONS; it has complications like the
following;
a. There is going to be an hemorrhagic effusion of the
pleura.
Pathophysiology cont
a. There will be sepsis
b. Ulcerations of the bowel
c. There will be hemorrhagic meningitis.
 Pathophysiology

Anthrax
3. Gastrointestinal anthrax
- this occurs through ingestion of meat that is poorly
cooked.
- The manifestations will be like ; pain in the
abdomen, bloody diarrhea, fever and vomiting
- It has been associated with a higher mortality.
 Laboratory diagnosis
1. Examination of blood agar; the blood smear is
made from the superficial vein of the ear of the
animal. It is then stained with gram’s or
polychrome methylene blue stain.
2. Isolation and identification of bacteria: this can be
isolated from heart blood and spleen of organisms
infected, from skin and hair.
1. The incubation period lasts for 18-24 hrs and then
growth occurs on blood agar. This is manifested
by morphology of grey/white , colonies that are
flat.
2. For cutaneous anthrax, the antibodies develop in
68%-92% of patients to both protective antigen
and to capsule.
Prevention
We have some ways of how we can prevent
bacillus anthracis from spreading anthrax;
These includes among many;
1. Vaccination of animal herds.
2. Humans should also be vaccinated (Ava
biothrax).
Treatment
1. Penicillin: It is susceptible to penicillin.
2. Prophylaxy: ciprofloxacin.
3. Tetracyclines: if we test this in animals it
indicate doxycycline is good. We use
chloramphenicol, gentamicin and
erythromycin for patients who has a
penicillin hypersensitivity.
Treatment cont
1. Fluoroquinolone, ciprofloxacin; this has
shown its effectiveness in monkeys and
guinea pigs and hence it can also be
effective to treat human anthrax.
 3. Bacillus cereus
This one has a similar morphology to B anthracis.
1. It is gram positive rod-shaped
2. Spore-forming facultative anaerobe.
3. They have peritrichous flagella involved in
locomotion and secretion of toxins
4. Some strains have a crystalline glycoprotein layer
(s-layer ) on the surface.
1. This covers the cell wall. They have a
protein within the s-layer to enhance
adhesion of B.cereus to host cells and also
providing resistance to gamma ray
radiation.
 Epidemiology
B. Cereus has been reported as an infection mainly
from food borne outbreaks of gastroenteritis
commonly in isolated countries. There’s limited data
of epidemiology on B. Cereus. This is due to;
1. Mild and short-duration of symptoms
2. The limiting nature of most B.cereus infections
(that actually means that individuals do not seek
medical assistance).
3. There is also lack of laboratory confirmation test.
Virulence factors of B. Cereus;
1. Toxins that form pore.
2. Cereulide, hemolysins, enterotoxins,
proteases and phospholipases.
 Epidemiology con’t
The centers for Disease Control reported that 619
outbreaks of bacillus cereus that were confirmed
related to poisoning from 1998 until 2015 that
involved 7385 illnesses. 75 illnesses and 3 deaths
were confirmed during that time. It also states that the
total outbreaks were 19119 and 373531 illnesses,
14681 hospitalized, 337 deaths cases.
This statistics also include other bacilli related
Illnesses.
In the FDA “ Bad Bug Book” reported an
estimated number of 63400 episodes of illnesses
annually in US. In 2007 to 2007, 13 outbreaks
confirmed and there were some suspected
outbreaks of about 37.6 that involved 1000
people.
Pathophysiology
Its pathogenicity is associated with
exoenzyme production.
Four hemolysins, three distinct
phospholipases, and three spore-forming
enterotoxins. Hemolysin BL(HBL), non
hemolytic enterotoxin and cytotoxic K are the
enterotoxins that activates nod-like receptor.
Vegetative cells that were ingested as viable
cells or spores, are the ones which produce or
secret a protein enterotoxin and also induce
diarrheal syndrome in the small intestine.
Cereulide is a plasmid encoded cyclic
peptide. It is produced in food products and
are ingested as formed toxins.
In diarrheal form, a three component of
nonhemolytic enterotoxin has been found.
This non hemolytic enterotoxin is the one
activating the nod-like receptor protein-3
inflammasome and pyroptosis. The result is a
programmed death of cells that was initiated
by the inflammatory caspases of the infected
Diagnosis
1. Hemolytic colonies
2. Lecithinase(+)
3. Resistant to penicillin
4. There’s lack of pathogenicity for mice.
5. Appendicitis
6. Diverticulitis
7. Mesenteric ischemia
1. Toxins by staphylococcus aureus.
2. Viral infections for example Rotavirus.
3. Infections from bacteria includes; campylobacter,
shigella, salmonella, Escherichia coli, Yersinia
enterocolitica, vibrio cholera, clostridium difficile.
4. Infections from parasites includes; Giardia,
cryptosporidium, Entameba, microsporidium, and
cyclospora.
Treatment
1. Vancomycin is the first choice for treating
B. Cereus
2. Symptomatic care with oral hydration.
3. Intravenous fluid hydration for patients
with severe cases.
4. Listeria monocytogenes
Listeria monocytogenes is a gram-positive
rod that is short and nonbranching. It does not
produce spores, facultative intracellular rod
bacteria that are catalase positive, and beta-
hemolytic when grown on blood agar. Only
L. monocytogenes, one of several Listeria
species, significantly contribute to human
disease.
Rarely do people with severe
immunosuppression become unwell after
exposure to L. ivanovii or L. gravi. The
gram-positive, facultative rod known as
Listeria monocytogenes is what causes
listeriosis, an infection. Due to the possibility
of contracting L. monocytogenes and
transmitting it to the fetus, pregnant women
Epidemiology
The Center for Disease Control (CDC) estimates
that every year, 1,600 people contract listeriosis,
and 260 of them pass away due to the illness.
Pregnant women, young children,
immunocompromised people, and the elderly are
most likely to contract the disease (65 and older).
Because it can be found in soil, water, and in
decomposing vegetation, L. monocytogenes is
extremely common. The human digestive
system contains the bacterium as well. The
following foods have the highest rates of
infections caused by L. monocytogenes:Fresh
sprouts, untainted milk, supple cheeses,icy deli
meats,chilly hot dogs,smoked seafood.
Pathophysiology
L. monocytogenes can develop in a refrigerator.
Low temperatures enhance the activity and
replication of L. monocytogenes by inducing
enzymes like RNA helicase. The ability of L.
monocytogenes to build biofilms improves its
resistance to hostile conditions. L. monocytogenes
uses flagella when the temperature is lower.
The longer the bacteria are exposed to higher
temperatures, the more likely they are to lose
their flagella. This process allows the bacteria
to propel itself and latch onto enterocytes
early in infection.
Once the infection has occurred, L.
monocytogenes can cause amnionitis, sepsis,
spontaneous abortion in pregnant women,
granulomatosis infantiseptica, and meningitis.
Healthy individuals infected with L.
monocytogenes typically have self-limiting
gastroenteritis with diarrhea and vomiting.
Diagnosis
A culture of the bacteria from the blood, cerebral
spinal fluid, or placental fluid is necessary to
diagnose L. monocytogenes. Listeria species
develops once inside the lab on a unique variety
of agar called Meuller-Hinton agar. Gram-
positive rods with beta-hemolytic colonies can
be identified through culture.
Treatment and control
Ampicillin or penicillin G administered intravenously
(IV) are the preferred antibiotic treatments. If the
patient has a penicillin allergy, trimethoprim-
sulfamethoxazole is a therapy option.
Avoiding commonly contaminated foods and washing
your hands properly are two ways to stop the spread
of L. monocytogenes.
 5. Actinomycetes
Actinomycetes are non-motile bacilli-shaped
microorganisms that are intermediate between
bacteria and fungi. They have a cell wall and
prokaryotic nucleus, giving them a bacterial
appearance, but they also generate filamentous
structures called hyphae. These hyphal structures
can be seen plainly on isolated culture media. They
are also gram-positive and catalase positive.
Epidemiology
Infections caused by Actinomycetes are common in
male than in female with a 4:3 ratio and largely
distributed world wide. They are more common
also in
● Individuals with poor dental hygiene
● Rural areas and farm workers
● Young and middle aged patients
Pathophysiology
Actinomycetes commonly cause an infection
known as the Actinomycosis infection.
Actinomycosis can present as cervicofacial
actinomycosis, thoracic actinomycosis (15-
20% of cases), and actinomycosis of the
abdomen and pelvic regions(accounts for 15-
20% cases of actinomycetes).
 Pathophysiology(Actinomycosis)
Actinomycosis infection is characterized by
● granulomatous inflammation,
● abscess formation,
● development of yellow/whitish granules
known as sulfur granules.
 Diagnosis
Cultured organism isolation and microscopy
techniques can be utilized to identify actinomyces
directly. Sputum, discharges, and infected tissue are
immediately transported to the lab, preferably under
anaerobic conditions, and may contain sulfur
granules, which are clearly visible under a
microscope.
 Diagnosis
The sulfur granules are isolated from the pus and
are usually yellowish or white in color with
different sizes. They are then crushed on a glass
slide and stained with Gram stain or Ziehl-Neelsen
staining procedures, decolorized with 1% sulfuric.
The stained smears are next examined under a
microscope for Gram-positive hyphal fragments
with a peripheral zone.
Treatment and control
Treatment for Actinomycosis includes mainly;
● High doses of Intravenous penicillin G(2-6
weeks)
● Oral penicillin v
● Surgical treatment in case of presence of necrotic
tissue
The main important technique for it prevention and
control are: Good dental and oral hygiene
Tropheryma Whipplei
The tropheryma whipplei is an actinomycete
bacteria commonly known for causing Whipple's
disease affecting the small intestine and it is gram-
positive upon staining. Furthermore the Whipple’s
disease can cause fever, abdominal pain,
diarrhea,weight loss, and involve the mesenteric
lymph nodes of the small intestine
 Laboratory diagnosis
● PCR test are done to identify the Tropheryma
Whipplei
● Specimen collected is a intestinal biopsy in which a
upon staining with the PAS stain they appear as
positive bacilli.
Treatment and control of Whipple’s disease
include;
● Penicillin, ampicillin, and tetracycline, doxycycline
plus for 1-2 years
● Hydroxychloroquine for 12-18 months
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