Selected human infectious diseases part 1

2.  AGE
 Newborns and older adults have reduced defenses against
infection
 HEREDITY
 Genetic susceptibility
 STRESS
 Stressors elevate blood cortisone. epinephrine
 NUTRITIONAL STATUS
 Adequate nutritional status will increase resistance to infection
 MEDICAL THERAPIES
 Chemotherapy and Radiotherapy decrease resistance
 CO-MORBID CONDITIONS
 Diabetes, COPD, Chronic Diseases will all weaken the defense
barriers

3. 1. Endoparasites
2. Ectoparasites

4. 1. Viruses:
- depends on host cell metabolism for their
replication
- obligate intracellular parasites
- Some do not cause any disease, some
cause acute illness (colds, influenza)
- Some cause lifelong latency and long term
reactivation (herpesviruses)
- Some cause chronic disease ( hepatistis B)

5. 2. Bacteriophages, Plasmids, Transposons)
- Mobile genetic elements that encode
bacterial virulence factors(adhesisns,
toxins or enzymes that confer antibiotic
resistance)
- Can infect bacteria and incorporate
themselves into their genome, thus
converting an otherwise harmless bacteria
into virulent one or an antibiotic sensitive
organism into a resistant one.

6. 3. Bacteria
- Next to viruses, they are the most frequent and
diverse class of human pathogens
4. Fungi
- Affecting the superficial layer of skin – tinea ,
dermatophytes
- Affecting the subcutaneous tissue – causing
abscesses or granulomas
- Deep fungal infection – systemic infection
- Oportunistic fungi - ( Candida, Mucor,
Aspergillus)

7. 5.Protozoa
example: Trichomonas vaginalis
Entamoeba histolitica
Giardia lamblia
6. Helminths – parasitic worms
Round worms – nematodes ( Ascaris)
Flatworms – cestodes ( pork and beef tapeworms)
Flukes – trematodes - leaf like worms ( liver and
lung flukes)

8. - Are arthropods ( lice, ticks, bedbugs, fleas
that attach to and live on the skin

9. 1. Intact host skin and mucosal surfaces and
secretory- excretory products example –
lysozyme , gastric juices
Respiratory tract
- Larger inhaled microbes are trapped in
mucociliary blanket of the upper airway passages
- Those that reached the trachea are either
coughed up or pushed backward toward the
throat by ciliary action, then swallowed and
cleared.
- -particle 5um or smaller in size reach the alveoli

10. Gastrointestinal tract
- Pathogens are transmitted by food or drink
contaminated with fecal material
Normal defenses Against Ingested
pathogens:
1. Acid gastric juice
2. The Viscous mucous layer covering the gut
3. Lytic pancreatic enzymes and bile
detergents
4. Secreted IgA antibodies

11. Urogenital tract
- Normally sterile
Skin
- dense, keratinized outer skin layer
- Low pH and the fatty acid content – favor
commensal bacteria

12. 1. They can contact or enter host cells and directly
cause cell death.
2. They may release endotoxins or exotoxins that
kill cells at a distance , release enzymes that
degrade tissue components, or damage blood
vessels and cause ischemic necrosis.
3. Induce host-cellular responses that may cause
additional tissue damage, including suppuration,
scarring, and hypersensitivity reactions.

13. Viral Respiratory Infections
- Most frequent, least preventable
- Self-limiting to life threatening
pneumonias
- May lead to superinfection with bacteria
- Most important and most studied:
rhinovirus and influenza virus

14.  50% common colds
 Member of picornavirus family (small RNA
viruses) which include poliovirus, hepatitis virus
and coxsackie virus
 Single -stranded RNA unecapsulated
 Infect humans and higher primates
 Infection confined to upper respiratory tract
(grow best at 33 C to 35 C)
 Induce serotype specific IgG and IgA antibodies

15.  Larger and more complex than rhinoviruses
 Single-stranded RNA
 Types: A, B, and C
Type A
- Infect humans, pigs, horses and birds and
are the major cause of pandemic and
epidemic flu infections.
- Antigenic shift

16. Type B and C
- Does not show antigenic shift or drift
- Infect mostly children who develops
antibodies against reinfection.

17. Haemophilus Influenzae Infection:
- Pleomorphic gram-negative organism
- Major cause of life-threatening acute lower
respiratory tract infections and meningitis in
young children.
- Major cause of suppurative meningitis in
children upto five years of age
- Purulent conjunctivitis in children
- Ubiquitous colonizer of the pharynx
5%- encapsulated
95% - unencapsulated

18.  Six serotypes of encapsulated form:
- A to F type b is the most frequent cause of
severe invasive disease.
- Nonencapsulated type:
- Produces otitis media
- Sinusitis and bronchopneumonia

19. Two species that cause tuberculosis:
1. Mycobacterium tuberculosis – transmitted by
inhalation
2. Mycobacterium bovis- transmitted by milk from
diseased cows and first produces intestinal or
tonsilar lesions.
3. *Mycobacterium leprae – causes leprosy

20.  MYCOBACTERIA
- Are aerobic, non-sporforming non-motile bacilli
with waxy coat that retain the red dye when
treated with an acid.
- Grow very slow ( 4 to 6 wks to obtain colony)

21. Primary tuberculosis –
- Begins with inhalation of the mycobactria
and ends up with a T-cell mediated immune
response that induces hypersensitivity to
the organisms
- Most often seen in the periphery of one lung
*Ghon complex – calcified scar in the lung
parenchyma and in the hilar lymphnode

22. Secondary and disseminated Tuberculosis
- Some individuals become reinfected with
mycobacteria
- Reactivate dormant disease
- Progress directly from primary mycobacterial
lesions into disseminated disease.
- * the granulomas most often occur in the apex
of the lungs but may be widely disseminated
in the lungs, kidneys, meninges, marrow and
other organ

40. Organs resistant to TB bacilli:
1. Heart
2. Striated muscle
3. Thyroid
4. Pancreas

41. *Miliary tuberculosis
- Refers to the hematogenous dissemination of
tuberculous lesions through out the body.
Frequent Cite:
Lungs, cervical lymphnodes (scrofula), meninges
Kidneys, adrenals, bones (osteomyelitis), fallopian
tubes, epididymis, vertebral TB (Pott’s dse.)
Resistant Cite:
Heart,Striated muscle,Thyroid gland and pancreas

42. Histoplasmosis and Coccidioidomycosis :
- Both are granulomatous disease of the lungs
- Both are caused by fungi that are thermaly
dimorphic.

43. Histoplasma capsulatum
- Is acquired by inhaalation of dust particles
from soil contaminated with bird or bat
droppings that contain small spores
(microconidia)n- the infectious form of the
fungus.

44. Clinical manifestations:
1. Coin lesion on the chest x-ray
2. Chronic , progressive secondary lung disease
which is localized to the lung apices and causes
cough, fever and night sweats
3. Localized lesions in extrapulmonary sites,
including mediastinum, adrenals, liver or
meninges
4. Widely disseminated involvement
(immunosuppressed)

45. Coccidioidomycosis
- Inhalation of the spores of Coccidioides
immitis
- Most are assymptomatic
- 10% with lung lesions, fever, cough and
pleuritic pains
- 1% disseminated C. Immitis involving the
meninges and skin

46. GARTROINTESTINAL (GI)
INFECTIONS

47. - Acute, self limiting infectious diarrhea
- Rotaviruses, Norwalk-like viruses,
coronaviruses and adenoviruses

48. Rotavirus-
- Major cause of diarrhea in infants
- Spread by fecal-oral route
- Invade and destroy mature host epithelial cells
in the middle and upper villus
- Older children and adults are resistant
- ( secretory immunity)
- Antirotavirus antibodies is present in mother’s
milk

49. Norwalk-like viruses
- Cause of epidemic gastroenteritis with
diarrhea, nausea, and vomiting among
children.
Coronaviruses
- Causes diarrhea and upper respiratory tract
infections and are usually endemic rather than
epidemic.

50. Enteric adenoviruses
- The second leading cause of diarrhea among
infants

51. SHIGELLA BACILLARY DYSENTERY
*dysentery – refers to diarrhea with abdominal
cramping and tenesmus in which loose stools
contain blood, pus and mucus.
- Caused by Shigella dysenteriae. S. Flexneri, S.
Boydii and S. Sonnei as well as certain O-type
of enterotoxic E. coli

52.  Transmission is fecal-oral route
 *S. flexneri is the major cause of bacillary
dysentery in endemic locations of poor
hygiene, including large regions of the
developing world and institutions in the
developed world.
 * epidemic shigellosis occurs when individuals
consume uncooked foods at picnics or other
events.

53. CAMPYLOBACTER ENTERITIS
- Comma shaped, flagelatted, gram –negative
organism
- Important cause of chronic gastritis,
enterocolitis, and septicemia
- Infection occurs by ingestion of contaminated
liquid or solid food such as milk, poultry, or
water.

54. - Epidemic cases affecting both children and
adults
- Sporadic infections may be derived from human
or zoonotic sources; domestic dogs are frequent
carriers.
Clinical manifestations:
1. Watery diarrhea( toxin-induced)
2. Bloody diarrhea ( invasion and proliferation
within the intestinal epithelium)
3. Enteric fever( organism penetrated the
intestinal mucosa)

55. SALMONELLOSIS AND TYPHOID FEVER:
Salmonella – are flagellated, gram negative
bacteria that cause a self limited food-borne
and water-borne gastroenteritis ( S.
enteritidis; S. typhimurium and others) or a
life threathening systemic illness marked by
fever (S. typhi)

56. Major source of contamination (other than S.
typhi)– feces contaminated meat and
chicken that are insufficiently washed and
cooked.
S. typhi – human is the only host which is
shed in the feces, urine, vomitus and oral
secretions by acutely ill persons and in the
feces by chronic carriers without overt
disease.

57. Clinical manifestations:
- Fever and chills during the first week
- Widespread reticuloendothelial involvement
with rash , abdominal pain, during the 2nd
week
- Ulceration of the Peyer’s patches with
intestinal bleeding at the 3rd week.
- * gallbladder colonization – causes a
chronic carrier state.

58. CHOLERA
- Caused by Vibrio cholerae
- Are comma shaped, gram –negative bacteria
- Causing severe watery diarrhea caused by an
enterotoxin secreted by 01-serotype V.
Cholerae and a non-01 sero-type causes
diarrhea associated with eating contaminated
shellfish
- *never invade the enteric epithelium but
instead remain within the lumen and secrete
their enterotoxin

59. AMEBIASIS
- Brought about by Entamoeba histolytica
- Protozoan parasite
- Major cause of dysentery and liver abscess
- E. histolytica cysts – infectious form of the
parasite because they are resistant to
gastric acid.

60. Amoeba dysentery
- Bloody diarrhea, intestinal pain, fever
- Frequently involves the cecum, and ascending
colon followed in order by the sigmoid, rectum
and the appendix.
- Fullblown cases – entire colon is involved.
- * flask-shaped ulcer – narrow neck and broad
base
- *Ameboma – napkin- like constrictive lesions

61. Amebic liver abscess:
- Chocolate –colored odorless, pasty materials
likened to be anchovy-paste
- May produce pain by pressing the liver
capsule as it enlarged.
- Treated with drainage and drugs or drugs
alone

62. GIARDIASIS
- Caused by Giardia lamblia – most prevalent
pathogenic intestinal protozoan worldwide.
- May be subclinical or may cause acute or
chronic diarrhea, steatorrhea, or
constipation.
- Endemic in public water supply

63. Infections Exists in Two forms:
1. A dormant by infectious cysts spread by
fecal-oral routefrom person to person (as
well as from cats, bears and beavers to
person)
2. Tropozoites that multiplyin instinal lumen
and cause disease.

64.  Giardia resides in the duodenum rather than
the colon
 Adhere to but do not invade intestinal
epithelial cells
 Cause diarrhea rather than dysentery.

65. GRAM-POSITIVE
PYOGENIC BACTERIAL
INFECTIONS

66. - Staphylococcus aureus – are pyogenic non-
motile, gram-positive cocci
- Skin lesions – boils, carbuncle, impetigo
and scalded skin
- Also cause pharyngitis, pneumonia,
endocarditis, food poisoning and toxic
shock syndrome

67.  S. aureus is the major cause of infection of
patients with burns and surgical wounds and
is second only to E. coli.
 *S. epidermidis - causes opportunistic
infections in catheterized patients, patient
with prosthetic cardiac valves, and drug
addicts.

68. Enzymes and toxins Secreted by S. aureus:
1. Staphylococci infecting prosthetic valves
and cathethers have an exopolysaccharide
capsule that allows them to attach to the
artificial matrials and to resists host cell
phagocytosis
2. The lipase of S. aureus degrades lipids on
the skin surface, and its expression is
correlated with the ability of the bacteria
to produce skin abscess.

69. 3. S. aureus enterotoxins are associated with food
poisoning and appear to act by stimulating
emetic receptors in the abdominal viscera and so
cause vomiting and diarrhea
4. Exfoliative toxins of S. aureus are associated with
staphylococcal scalded-skin syndrome – forming
skin blisters.
5. Toxic shock syndrome toxin (TSST-1) is secreted
by S.aureus colonizing the vagina of women using
tampons causing shock by mechanisms similar to
those of S. Aureus enterotoxins.

70. - Are facultative anaerobic gram-positive cocci
- Cause suppurative infections of the skin,
oropharynx, lungs, and heart valve and also
cause poststreptococcal syndromes including
rheumatic fever, immune complex
glomerulonephritis, and erythema nodosum

71. -Most streptococci are beta-hemolytic
- S. pyogenes (Group A)- which causes
pharyngitis, scarlet fever, erysipelas, impetigo,
rheumatic fever and glomerulonephritis
- S. agalactiae (group B) – causes neonatal sepsis
and urinary tract infections.
- S. faecalis – (group D) – causes endocarditis and
urinary tract infections
- S. viridans – which is alpha-hemolytic and thus
green in blood agar plates – can cause
endocarditis

72. Streptococcus pneumoniae (pneumococcus) –
major cause of community –acquired
pneumonia and major cause of bacterial
meningitis in adults.
*Streptococcus mutans – is the major cause of
dental caries.

73. Virulence factor of Streptococci:
• M-protein – a rod like surface protein that
prevents bacteria from being phagocytosed.
• Pyrogenic exotoxin – causes fever and rash in
scarlet fever
• S. mutans produces caries by metabolizing
sucrose to lactic acid
• Poststreptococcal autoimmune diseases of the
heart (rheumatic fever) may result from
antistreptococcal M-protein antibodies that cross
react with cardiac myosin.

74. ANAEROBIC
BACTERIAL
INFECTIONS

75. - Gram-positive bacilli that grow under
anaerobic conditions and produces spores
which are frequently present in the soil.

76. Four Types of Clostridium:
1. C. perfringens (welchii), C. septicum and other
species invade traumatic and surgical wounds
and cause an anaerobic cellulitis or myonecrosis
(gas gangrene)
- Contaminate illegal abortions and cause
uterine myonecrosis, cause mild food poisoning
2. C. tetani – proliferates in puncture wounds and
in umbilical stump of the new born- release a
potent neurotoxin tetanospasmin that causes
convulsive contractions of skeletal muscles.

77. 3. C. botulinum – grows in inadequately
sterialized canned foods and releases a potent
neurotoxin that block synaptic released of
acetylcholine and causes a severe paralysis of
respiratory and skeletal muscles.
4. C. difficile – overgrows other intestinal flora
in antibiotic-treated patients, release multiple
toxins, and cause pseudomembranous colitis

79.  Folliculitis is an infection of the hair follicles
and produces a number of small
erythematous or pustular lesions .
 It is usually caused by Staphylococcus
aureus.
 Local warm compresses and topical
antibiotics are all that is needed as therapy.

80.  A particular form of folliculitis occurs in
persons who have bathed in swimming
pools or whirlpool baths contaminated by
Pseudomonas aeruginosa
 A pruritic papulopustular rash, those
covered by a bathing suit (the buttocks,
hips, axillae and the lateral side of the
trunk), develops within a day or two of
exposure.
 no therapy is required and topical steroids
should be avoided.

81. Small red lesion, each associated with a hair follicle and caused by
Staphylococcus aureus.

82. Pseudomonas folliculitis. Papulopustular rash over the buttocks and thighs
following use of a spa pool.

83.  A furuncle (boil) is a S. aureus infection of an
obstructed hair follicle.
 It begins as a red, tender, inflammatory
nodule on the face, neck, axilla or other area
of hairy skin.
 Constitutional symptoms and fever are not
common.
 Antibiotic therapy is not usually necessary;
surgical drainage or the application of warm
soaks is all that is normally required.

84.  Patients with diabetes, poor hygiene and
excessive sweating may suffer from
recurrent furuncles.
 Antibiotic ointment to the nares and/or the
use of systemic rifampicin may eradicate
carriage.

85. Small cutaneous abscess associated with hair follicle on back of neck.

86.  A carbuncle is a larger abscess (almost
always staphylococcal) extending from an
infected follicle into the subcutaneous fat.
 It is often seen at the nape of the neck , or
on the back.
 Carbuncles require surgical drainage and
treatment with an anti-staphylococcal
antibiotic.

87. A huge area of induration of the neck with multiple discharging follicular
abscesses.

88.  chronic, suppurative infection of apocrine
sweat glands is fortunately rare.
 It is often due to S. aureus, and occurs
principally in adults.
 It results in recurrent crops of abscesses,
leading to sinus formation.
 Oral anti-staphylococcal therapy combined
with moist compresses and drainage of
fluctuant lesions.

89. Extensive scarring with multiple sinuses in and around the axilla.

90.  Impetigo is a superficial streptococcal or
staphylococcal infection of the skin.
 It is highly communicable; transmission is
enhanced by low socioeconomic status with
its associated poor living conditions and
hygiene.
 The organisms probably cannot invade
intact skin - infection occurs through minor
abrasions, insect bites, etc.
 The infection often spreads rapidly
presumably by scratching and
autoinoculation.
 It may also complicate eczema or varicella.

91. Impetigenized eczema. Young Asian child with severe atopic eczema
secondarily infected with impetigo.

92.  All impetigo is initially vesicular, later
becoming crusted; depend on whether the
aetiological agent is Streptococcus pyogenes
or S. aureus .
 After rupture, the discharge dries to form
characteristic thick, adherent, golden-yellow
crusts.
 Staphylococcal impetigo, on the other hand,
typically produces more long-lived bullae and
thin, light brown crusts (described as `varnish-
like').

93. Streptococcal impetigo. The cluster of superficial vesicles has broken to form
a row weeping surface, soon to be covered by a yellow crust.

94. These characteristic yellow
crusts are often the main
feature on presentation.

95. Severe streptococcal impetigo
crusts over the face of a young girl.

96. Adherent dark yellow/brown
crust of impetigo in fingers.

97. Bullous impetigo. Lesions on
finger and wrist.

98.  The cause of impetigo can be determined
by Gram stain or by culture of the exudate
beneath the crust.
 Anti-DNAase B and anti-hyaluronidase
titres usually rise after streptococcal skin
infection, but the anti-streptolysin O (ASO)
titre often does not.

99.  Certain strains of B-hemolytic streptococci
- the so-called nephritogenic strains - may
give rise to immunologically-mediated
acute post-streptococcal nephritis after
skin infection

100.  There are two approaches to the antibiotic
treatment of impetigo.
 One is to use penicillin alone (or
erythromycin in the penicillin-allergic
individual
 The other approach is to use an anti-
staphylococcal antibiotic

101.  Systemic antibiotics are more effective than
topical therapy
 Injudicious treatment with steroid skin
creams removes the crusts but promotes
spread of the infection, with numerous red
raw lesions.

102.  Cellulitis is a spreading superficial infection
of the skin.
 due to streptococci or S. aureus.

103.  Infection can occur at any age
 often develops at a site of previous trauma
or skin lesion, the entry site may be
unapparent.
 Patients frequently have an abrupt onset of
malaise, fever, chills and headache and the
involved skin becomes tender, red, warm
and swollen.

104. Erythematous area with ill – defined margin over lower limb.

105.  The inflammation spreads with poorly
defined margins and may be accompanied
by lymphangitis and lymphadenopathy.
 Streptococcal cellulitis occasionally
becomes bullous.

106. A severe rapidly developing infection of the subcutaneous
tissue of the leg with large bullae and scabs.

107. Large bullae in an area of cellulitis of the neck caused by
Streptococcus pyogenes.

108.  The diagnosis of cellulitis is usually a
clinical one
 Gram stain or culture of material aspirated
from the leading edge of the cellulitis.

109. Chains among streptococci among cellular debris in pus.
Gram’s stain.

110.  if there are no initial clues to the aetiology then a
penicillinase-resistant penicillin should be given
(e.g. flucloxacillin 0.5-1.0g orally every 6 hours).
 For the more severely ill patient parenteral therapy
may be needed and for the penicillin-allergic
individual, erythromycin or clindamycin would be
suitable.

111.  In children an unusual form of cellulitis may
be caused by Haemophilus influenzae type b.
 It is commonly seen on the cheek and
produces a purple-red, bruised appearance .

112. Cellulitis due to haemophilus
influenzae of the cheek and
preorbit.

113.  Following laceration or trauma during
swimming in fresh water and seawater
 A severe form of cellulitis, often complicated
by necrosis and bacteraemia

114. Severe infection with bullous
lesions due to Vibrio vulnificans
infection following immersion of
leg in brackish water.

115. Vibrio Cellulitis. Haemorrhagic bullous lesions of Vibrio
vulnificans sepsis.

116. Comma-shaped cells of Vibrio vulnificans. Gram’s stain.

117.  Erysipelas is a characteristic variant of cellulitis,
almost always caused exclusively by S. pyogenes.
 It is a painful, bright red, shiny lesion with a raised,
sharply demarcated, advancing edge .
 It is most common on the legs or face and often
spreads across the nose to involve both cheeks (the
`butterfly-wing' rash ).

118. Well demarcated area of erythema and induration on the
forehead.

119. A typical butterfly-wing rash on the cheeks. Both eyes are
closed by oedema of the lids.

120.  With high fever and rigors and a leucocytosi.
 Erysipelas is treated with penicillin, given
parenterally in the more severe cases.

121.  Scarlet fever
 Some group A haemolytic streptococci produce an
erythrogenic toxin causing the characteristic rash of scarlet
fever. Infection is usually of the pharynx or tonsils although
streptococcal skin or wound infection can also be associated
with scarlet fever. The rash of scarlet fever begins on the face
, neck and upper chest, spreading to the abdomen and
extremities: it consists of a diffuse scarlet erythema with
almost confluent punctate papules. This is called punctate
erythema.

122. Scarlatina. The face appears flushed with circumolar pallor.

123.  There is often also slight prominence of the hair
follicles, giving a sandpaper-like texture to the skin.
The rash blanches upon pressure . The erythema
often spares the area around the mouth but is
accentuated in the creases of the elbows, groin and
axillary folds (Pastia's lines). The tongue is at first
furred with prominent papillae (the `white
strawberry' tongue). After about 4 days there is
extensive desquamation of the skin which may
continue for 2 weeks or more.

124. Diffuse erythematous rash
showing blanching where finger
pressure has been applied to the
abdomen.

125. Extensive desquamation of the skin of the trunk. This may
last for several weeks.

126.  Desquamation of the tongue also occurs
leaving a raw, red tongue with prominent
papillae (`red-strawberry' tongue).
 Culture of a swab from the throat or from the
infected wound will demonstrate group A b-
haemolytic streptococci. The condition is
treated with penicillin.

127.  Toxic shock syndrome (TSS) is mediated by
one or more of the exotoxins produced by S.
aureus.
 It occurs predominantly in menstruating
females using tampons
 but can occur with staphylococcal infection at
other sites and in males or children.

128.  The rash is a diffuse, blanching, macular
erythema, particularly affecting the hands
and feet, which desquamates 1-2 weeks after
it appears.

129. Typical sunburn-like rash over the face and trunk. Note the
dryness and hyperaemia of the lips.

130. Desquamation of the skin, particularly of the palms and
soles, occur with recovery.

131.  The diagnosis of TSS is clinical and the
isolation of S. aureus is not necessary.

132.  The initial treatment should be with
aggressive supportive care.
 Intravenous anti-staphylococcal antibiotics
are also given but
 Antibiotic therapy is usually given for 10-14
days
 Women who have had TSS should not use
tampons again.

133. Certain strains of S. aureus produce an exfoliative
exotoxin, release of which may cause a
syndrome termed staphylococcal scalded skin
syndrome (SSSS), or Ritter's disease.
In neonates it is also termed pemphigus
neonatorum. It usually occurs in children and
starts with fever and a tender scarlatiniform
rash.

134.  Within a day or two, large flaccid, clear bullae
develop and exfoliation of sheets of skin
(resembling cigarette paper) occurs, leaving a
red, denuded base .
 Lateral traction of the skin causes it to
wrinkle and be displaced (a positive
Nikolsky's sign).