continuation of disease causing bacteria

1. MICROBIOLOGY I
(PPAS 241)
Kwabena Oppong

2. 2
BACTERIAL DISEASES OF HUMANS

3. 3

4. 4
Pathogenicity
• Pathogenicity is the capacity of a microorganism to
initiate disease.
• It requires the attributes of transmissibility or
communicability from one host or reservoir to a fresh
host, survival in the new host, infectivity or the ability to
breach the new host’s defenses, and virulence, a variable
that is multifactorial and denotes the capacity of a
pathogen to harm the host.
• Virulence in the clinical sense is a manifestation of a
complex bacterial–host relationship in which the
capacity of the organism to cause disease is considered in
relation to the resistance of the host.

5. 5
Types of bacterial pathogens
• Bacterial pathogens can be classified into two broad groups, primary and
opportunistic pathogens.
• Primary pathogens are capable of establishing infection and causing disease in
previously healthy individuals with intact immunological defenses. However, these
bacteria may more readily cause disease in individuals with impaired defenses.
• Opportunistic pathogens rarely cause disease in individuals’ with intact
immunological and anatomical defenses. Only when such defenses are impaired
or compromised, as a result of congenital or acquired disease or by the use of
immunosuppressive therapy or surgical techniques, are these bacteria able to
cause disease.
• Many opportunistic pathogens, e.g. coagulase negative staphylococci and
Escherichia coli, are part of the normal human flora and are carried on the skin or
mucosal surfaces where they cause no harm and may actually have beneficial
effects, by preventing colonization by other potential pathogens.
• However, introduction of these organisms into anatomical sites in which they are
not normally found, or removal of competing bacteria by the use of broad-
spectrum antibiotics, may allow their localized multiplication and subsequent
development of disease.

6. 6
Pathogenesis of Bacterial Infection
• Steps involved in the pathogenesis of the bacteria:
1. Transmission
2. Colonization
3. Adhesion
4. Invasion
5. Survival in the host
6. Tissue Injury

7. 7
Transmission
• Potential pathogens may enter the body by various routes, including the
respiratory, gastrointestinal, urinary or genital tracts.
• Alternatively, they may directly enter tissues through insect bites or by
accidental or surgical trauma to the skin. Many opportunistic pathogens
are carried as part of the normal human flora, and this acts as a ready
source of infection in the compromised host (e.g. in cases of AIDS or when
the skin barrier is breached).
• Depending on the route of transmission, an infection could be described
as:
• Air-borne
• Food-borne
• Water-borne
• Sexually transmitted etc.

8. 8
Colonization
• The establishment of a stable population of bacteria on the
host’s skin or mucous membranes is called colonization.
• For many pathogenic bacteria, the initial interaction with host
tissues occurs at a mucosal surface and colonization normally
requires adhesion to the mucosal cell surface.
• This allows the establishment of a focus of infection that may
remain localized or may subsequently spread to other tissues.
Adhesion
• Adhesion is necessary to avoid innate host defense mechanisms such as
peristalsis in the gut and the flushing action of mucus, saliva and urine, which
remove non-adherent bacteria. For bacteria, adhesion is an essential
preliminary to colonization and then penetration through tissues.
• At the molecular level, adhesion involves surface interactions between specific
receptors on the mammalian cell membrane (usually carbohydrates) and
ligands (usually proteins) on the bacterial surface. The presence or absence of
specific receptors on mammalian cells contributes significantly to tissue
specificity of infection.

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Invasion
• Invasion is penetration of host cells and tissues (beyond the skin and
mucous surfaces), and is mediated by a complex array of molecules, often
described as ‘invasins’.
• These can be in the form of bacterial surface or secreted proteins which
target host cell molecules (receptors).
• Once attached to a mucosal surface, some bacteria, e.g. Corynebacterium
• diphtheriae or Clostridium tetani, exert their pathogenic effects without
penetrating the tissues of the host. These produce biologically active
molecules such as toxins, which mediate tissue damage at local or distant
sites.

10. 10
Survival in the host
• Many bacterial pathogens are able to resist the cytotoxic action of plasma and
other body fluids involving antibody and complement (classical pathway) or
complement alone (alternate pathway) or lysozyme.
• Killing of extracellular pathogens largely occurs within phagocytes after
opsonization (by antibody and/ or complement) and phagocytosis.
• Circumvention of phagocytosis by extracellular pathogens is thus a major
survival mechanism. Capsules (many pathogens), protein A (S. aureus) and M
protein (S. pyogenes) function in this regard.
• Intracellular pathogens (both obligate and facultative) must be able to avoid
being killed within phagolysozomes. This can occur from by-passing or lysing
these vesicles and then residing free in the cytoplasm.
• Alternatively, they can survive in phagosomes (fusion of phagosomes with
lysosomes may be inhibited or the organism may be resistant to degradative
enzymes if fusion with lysosomes occurs).

11. 11
TISSUE INJURY
• Bacteria cause tissue injury primarily by several distinct mechanisms
involving:
• Exotoxins
• Endotoxins
• Activities of the immune system (Immunopathology)

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Exotoxins
• Exotoxins are proteins produced some bacteria that modify, or destroy certain cellular
structures by enzymatic action.
• Effects of exotoxins are usually seen acutely, since they are sufficiently potent that
serious effects (e.g. death) often result. Examples of this are botulism, anthrax, cholera
and diphtheria.
• If the host survives the acute infection, neutralizing antibodies (anti-toxins) are often
elicited that neutralize the affect of the exotoxin.
• Classes of exotoxins include:
• Toxins that act on the extracellular matrix of connective tissue e.g. Clostridium
perfringens collagenase, Staphylococcus aureus hyaluronidase.
• Toxins that have a cell binding “B” component and an active “A” enzymatic component
(A-B type toxins)
• These include:
a) Those with ADP-ribosylating activity e.g. cholera toxin, E. coli heat labile toxin,
Pseudomonas aeruginosa and diphtheria toxins.
b) Those with a lytic activity on 28S rRNA e.g. shiga and shiga-like (vero) toxins.
c) Those with a partially characterized site of action e.g. botulinum toxin, tetanus toxin
and anthrax lethal toxin.

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Endotoxins
• Endotoxins are toxic components of the bacterial cell envelope. The
classical and most potent endotoxin is lipopolysaccharide. However,
peptidoglycan displays many endotoxin-like properties.
• Certain peptidoglycans are poorly biodegradable and can cause chronic as
well as acute tissue injury. Endotoxins are “non-specific” inciters of
inflammation.

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IMMUNOPATHOLOGY
• Immunopathology is the study of various diseases in which humoral (body
fluid) and cellular immune factors play a role in causing pathological
damage to cells, tissues, and the host. Defective or malfunctioning immune
responses often lead to illness or disease.
• Over stimulation of cytokine production and complement activation by
endotoxins can cause tissue injury in the absence of an immune response.
• Continuously generated antigens released from persisting viable microbes
will subsequently elicit humoral antibodies and cell mediated immunity
resulting in chronic immunopathology.
• Certain poorly degradable antigens (e.g pneumococcal polysaccharide and
group A streptococcal cell walls) can maintain immunopathology even in the
absence of persistence of live agents.
• Other bacterial antigens cross-react with host tissue antigens causing the
development of autoimmunity (e.g. the M protein of S. pyogenes cross-
reacts with mammalian myosin).
• Thus immunopathology can persist even after the infection and microbial
antigens are eliminated.

15. CHOLERA
• Cholera is an acute diarrheal illness caused by infection of the intestine
with Vibrio cholerae bacteria. People can get sick when they swallow
food or water contaminated with cholera bacteria.
• Incubation period:The incubation period of cholera is between 2 hours
and 5 days.
• Modes of transmission of cholera;
• A person can get cholera by drinking water or eating food
contaminated with cholera bacteria. In an epidemic, the source of the
contamination is usually the feces of an infected person that
contaminates water or food. The disease can spread rapidly in areas
with inadequate treatment of sewage and drinking water.

16. Signs and symptoms of cholera
• profuse watery diarrhea, sometimes described as “rice-
water stools”
• vomiting.
• thirst.
• leg cramps.
• restlessness or irritability.

17. Prevention of cholera
• Make sure to drink and use safe water to wash and prepare food, and
make ice.
• Wash your hands often with soap and running water
• Use latrines or bury your poop. Avoid open defecation
• Cook food well (especially seafood), keep it covered, and eat it hot,
where necessary.
• In general, practicing effective hand and environmental hygiene is the
best way to prevent cholera.

18. Complications of cholera
• Changes in breathing patterns
• Altered mental state
• Skin that, when pinched, doesn't immediately go back into place
• Kidney failure
• Loss of consciousness
• Shock
• Coma
• Death
Treatment includes
Rehydration, IV fluids and antibiotics.

19. PERTUSSIS / WHOOPING COUGH
• Pertussis is an acute, highly contagious disease which is
characterized by uncontrollable coughing, that is violent and
persistent.
• The coughing is followed by a sharp, high pitched intake of air
which create the characteristic “WHOOP” sound.
• Causative Agent:
• Bordetella Pertussis (Gram-negative, aerobic encapsulated
coccobacillus)

20. INCUBATION PERIOD
• The incubation period is typically seven to ten days in infants or
young children, after which there are usually mild respiratory
symptoms, mild coughing, sneezing, or runny nose.
MODE OF TRANSMISSION
• Tiny droplets that comes from mouth & nose of infected
patient.
• It is easily spread through the cough, especially when people
are in close contact with an infected person.

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• B. pertussis is a fastidious, gram-negative bacterium requiring special media for
isolation.
• B. pertussis produces multiple antigenic and biologically active products
including:
• Pertussis toxin
• Filamentous hemagglutinin (FHA)
• Agglutinogens
• Adenylate cyclase
• Pertactin
• Tracheal cytotoxin
• These products are responsible for the clinical features of pertussis. An immune
response to one or more of them produces immunity following infection. Some
observational studies suggest that pertussis infection can provide immunity for 4
to 20 years, but that it is not life-long.

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Pathogenesis
• Pertussis is primarily a toxin-mediated disease. The bacteria
• Attach to the cilia of the respiratory epithelial cells
• Produce toxins that paralyze the cilia
• Cause inflammation of the respiratory tract, which interferes with
the clearing of pulmonary secretions
• Until recently, scientists thought that B. pertussis did not invade the
tissues. However, recent studies suggest that the bacteria are present
in alveolar macrophages

23. 23

24. COMPLICATIONS
• Pneumonia
• Hypoxic encephalopathy
• Otitis media
• Tuberculosis activation
• Epistaxis, hemoptysis
• Hernia
• Reinduction of paroxysmal coughing with upper respiratory
infections
• Seizures
• Cerebral hemorrhage
• Coma and death

25. PREVENTION & CONTROL
• Active immunization is best preventive measure for pertussis. DTP
(Diphtheria, Tetanus, Pertussis) Vaccine
• DTP 1st
dose - 6 weeks
• 2nd
dose - 10 weeks
• 3rd
dose - 14 weeks
• 1st
Booster - 16th
-18th
month
• 2nd
Booster - 5 Years.
ANTIBIOTICS
• Erythromycin
• Azithromycin
• Clarithromycin

26. GONORRHOEA
• Causative organism: Neisseiria gonorrhoeae
• Incubation period: from time of exposure to the bacteria until
symptoms develops, is usually 2 to 5 days but sometimes the
symptoms may not develop up to 30 days or even until the
infection spread to othe areas of the body
• Mode of transmission: by having unprotected sex
• By mothers to babies by pregnancy or labour
• Signs and symptoms: painful urination, abnormal discharge from
penis and vagina, men may experience testicular pain, women may
experience pain in the lower abdomen, sores around the penis and
vagina itching.
• NB: sometimes gonorrhoea has no symptoms.

27. Complications
• Infertility in both men and women, infections that spread to joints and
other areas of the Body, complications in babies, increase risk of HIV/AIDS.
• Prevention: To reduce your chance of having gonorrhoea use condom if
you have sex.
• Abstaining from sex or adultery is the surest way to prevent gonorrhoea

28. MANAGEMENT
• In adults: adults with gonorrhoea are treated with antibiotics. Due to the
emerging strain drug-resistant neisseiria gonorrhoea, the Center for
disease control recommend that uncomplicated gonorrhoea can be
treated with antibiotic ceftriaxone.
• Patients allergic to cephalosporin antibiotics such as ceftriaxone are
given oral semifloxacin or injectable gentamicin and oral azithromycin.
• Partners: Your partner should also go through testing and treatment for
gonorrhoea if he or she has no symptoms of gonorrhoea and must
receive the same treatment as you do.
• Babies born to mothers with gonorrhoea who develop the infection can
be treated with antibiotics.

29. SYPHILIS
• Syphilis is a highly contagious disease that is mostly spread through sexual
activity. The infected person often doesn ot know that they have the
disease and passes it on to their sexual partner.
• Causes of Syphilis
• Syphilis is caused by the bacteria Treponema pallidum. You get it through
direct contact with a syphilis sore on someone else’s body.
• This usually happens during sexual activity, but the bacteria can also get
into the body through cuts on the skin or through mucous membranes.

30. Symptoms of Syphilis
Early or primary syphilis:
• People with primary syphilis get one or more sores called chancres. They are
usually small, painless ulcers. They happen on the genitals, anus or rectum, or in
or around the mouth between 10 and 90 days (3 weeks on average) after
exposure to the disease.
• Even without treatment, the ulcers heal without a scar within 6 weeks. However,
treatment keep the disease from moving to the next stage.
• Secondary syphilis: This stage begins 6 weeks to 6 months after initial exposure.
It may last 1 to 3 months.
• People with secondary syphilis usually get a rosy “copper penny” rash on the
palms of their hands and soles of their feet. They may also have different rashes
on other parts of their body.
• These may look like rashes caused by other diseases. People may have moist,
wart-like lesions in their groin, white patches on the inside of their mouth,
swollen lymph glands, fever, hair loss, and weight loss.
• As with primary syphilis, symptoms of secondary syphilis gets better without
treatment.

31. Symptoms of Syphilis
• Tertiary syphilis: If the infection is not treated, it may move on
to a stage marked by severe problems with the heart, brain,
and nerves.
• Other complications include paralyses, blindness, deafness,
dementia or impotence. It could even lead to death.

32. Complications Associated with Syphilis
• Small bumps; Bumps can grow on the skin and destroy the tissue around
them.
• Nervous system problems; Syphilis can cause problems like headaches,
meningitis, brain damage, paralysis, or hearing and vision loss.
• Cardiovascular problems; The disease can damage heart valves or cause
bulging blood vessels (aneurysms) or an inflamed aorta (aortitis).
• HIV; Syphilis can increase the chances of getting HIV.

33. TREATMENT FOR SYPHILIS
• Penicillin or doxycycline
• Avoid sexual interactions until treatment is completed
• Some people with syphilis have an immune system reaction called a
Jarisch-Herxheimer reaction several hours after their first treatment. This
might include fever, chills, headache, upset stomach, rash, or joint and
muscle pain but these problems usually go away within 24 hours.

34. BOTULISM
• Botulism is a rare but serious condition caused by toxins from bacteria
called Clostridium botulinum.
• The toxin causes paralysis, which starts in the face and spreads to the
limbs. If it reaches the breathing muscles, respiratory failure can result.
Incubation Period
• The average incubation period is 12 to 72 hours after the ingestion
• Botulism is not transmitted from person to person. It is spread by
consuming food contaminated with the botulism toxin or spores.

35. TYPES OF BOTULISM
• Foodborne botulism: Foodborne botulism is caused by consumption of
foods contaminated with botulinum toxin.
• C. botulinum grows and elaborates toxin only when the food presents
conditions that include an anaerobic environment, a pH of <4.5, low salt
and sugar content, and a temperature of 4°C–121°C.
• Wound botulism: Wound botulism is caused by contamination of a
wound with C. botulinum spores from the environment and subsequent
germination of these spores and production of toxin in the anaerobic
milieu of an abscess.

36. • Infant botulism. Infant botulism results from absorption of toxin
produced in situ by C. botulinum colonization of the intestines of certain
infants aged <1 year. This is the most common form of botulism, with
80–100 cases reported annually in the United States . Colonization is
∼
believed to occur because normal bowel florae that could compete
with C. botulinum have not been fully established.
• Studies have implicated honey consumption as a risk factor for illness,
but honey consumption probably accounts for only up to 20% of cases.
• The clinical presentation resembles that of adult forms of disease, with
common symptoms that include inability to suck and swallow, weakened
voice, and floppy neck and that may progress to generalized flaccidity
and respiratory compromise.

37. • iatrogenic botulism: Iatrogenic botulism is caused by injection of
botulinum toxin for cosmetic or therapeutic purposes. Doses
recommended for cosmetic treatment are too low to cause systemic
disease. Higher doses injected for treatment of muscle movement
disorders have caused anecdotal cases of systemic botulism-like
symptoms. Injection of unlicensed, highly concentrated botulinum
toxin caused severe botulism in 4 patients who received it for
cosmetic purposes.