13 - Microbial Diseases, Detection and Control

Microbial diseases,
detection and control

The progress of an infection
1. Portals of entry
-skin, gastrointestinal tract, respiratory tract,
urogenital tract
-inoculum size
2. Attaching to the host
-adhesion : fimbriae, surface proteins, capsules,
receptors, suckers, hooks, barbs
3. Surviving the host
Course of Infectious Disease
• incubation period
– period after pathogen entry but before signs
and symptoms appear
• prodromal stage
– onset of signs and symptoms
– not clear enough for diagnosis
• period of illness
– disease is most severe and has characteristic
signs and symptoms
• convalescence
– signs and symptoms begin to disappear
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3
required for reproduction or
Pathogen Transmission
• four main modes of transmission
– airborne
– contact
– vehicle
– vector borne

4
Virulence
• degree or intensity of pathogenicity
• virulence factors
– determine the degree to which the pathogen
causes damage, invasion, infectivity
• determined in part by pathogen’s ability to
survive outside host

5
Adherence and Colonization
• first step in infectious disease is entrance and attachment
• portal of entry
– skin, respiratory, gastrointestinal, urogenital systems, or
conjunctiva of eye
-vector borne, sexual contact, blood transfusion, or organ
transplant
• adherence
– mediated by special molecules or structures called adhesins
• colonization
– establishment of a site of microbial reproduction on or
within host
– does not necessarily result in tissue invasion or damage
6
Attachment and Colonization…
• adherence structures
– pili, fimbriae, specialized adhesion molecules on
bacterium’s cell surface bind complementary receptor sites
on host cell surface
– are a type of virulence factor
• colonization
– establishment of a site of microbial reproduction on or
within host
– does not necessarily result in tissue invasion or damage
7
Figure 31.8

8
Toxigenicity
• toxigenicity
– ability to produce toxins
• intoxications
– diseases that result from entry of a specific
preformed toxin into host
• toxin
– specific substance that damages host
• toxemia
– condition caused by toxins in the blood of host
9
Exotoxins
• soluble, heat-labile, proteins
• usually released into the surroundings as
bacterial pathogen grows
• most exotoxin producers are gram-negative
• often travel from site of infection to other
tissues or cells where they exert their effects

10
Endotoxins
• lipopolysaccharide in gram-negative cell
wall can be toxic to specific hosts
– called endotoxin because it is bound to
bacterium and released when organism lyses
and some is also released during multiplication
– toxic component is the lipid portion, lipid A

11
Endotoxins…
• heat stable
• toxic (nanogram amounts)
• weakly immunogenic
• generally similar, despite source
• cause general system effects
– fever, weakness, diarrhea, inflammation,
intestinal hemorrhage, and fibrinolysis, the
enzymatic breakdown of fibrin, the major
protein component of blood clots
12
Differential characteristics of bacterial
exotoxin and endotoxin
Characteristic Exotoxins Endotoxins
Toxicity Toxic in minute amounts Toxic in high doses
Effects on the body Specific to a celltype (blood, Systemic: fever, inflammation
liver, blood)
Chemical composition Small proteins Lipopolysaccharide of cell wall
Heat denaturation Unstable Stable
Toxoid formation Can be converted to toxoid Cannot be converted to toxoid
Immune response Stimulate antitoxins Does not stimulate antitoxins
Fever stimulation Usually not Yes
Manner of release Secreted from live cell Released by cell via shedding
or during lysis
Typical source A few gram positive and All gram negative bacteria
gram negative
Mycotoxins
• secondary metabolites of fungi

– common contaminants of food crops
– Aspergillus flavus and A. parasiticus produce
carcinogenic aflatoxin
– Stachybotrys produce tissue damaging
satratoxins
– Claviceps purpurea (ergot) produce
hallucinogen lysergic acid

14
Exiting the Host
• must occur if microbe is to be perpetuated
• active escape
– movement of pathogen to portal of exit
• passive escape
– excretion in feces, urine, droplets, blood,
saliva, or desquamated cells
– viremia spread of viruses in the blood

15
Host Resistance Overview
• most pathogens (disease causing microbes)
– must overcome surface barriers and reach
underlying
– overcome resistance by host
• nonspecific resistance
• specific immune response

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16
Immune response
1. Nonspecific immune response
– also called nonspecific resistance, innate immunity, and natural
immunity
– acts as a first line of defense
– offers resistance to any microbe or foreign material
– lacks immunological memory
2. Specific immune response

– also called acquired immunity, adaptive immunity, and specific
immunity
– resistance to a particular foreign agent
– has “memory”
• effectiveness increases on repeated exposure to agent
• the two types of responses usually work together
17
Host Defenses

18
Nonspecific (Innate) Host
Resistance
Physical Barriers in Nonspecific (Innate)
Resistance
• effectiveness impacted by:

– direct factors
• nutrition, physiology, fever, age, and genetics
– indirect factors
• personal hygiene, socioeconomic status, and living
conditions

20
Skin
• strong mechanical barrier to microbial
invasion
– keratin produced by keratinocytes in outer layer
• inhospitable environment for microbes
– attached organisms removed by shedding of
outer skin cells
– pH is slightly acidic
– high NaCl concentration
– subject to periodic drying

21
Mucous Membranes
• form protective covering that resists
penetration and traps many microbes
• are often bathed in antimicrobial secretions
which contain a variety of antimicrobial
substances

22
Antimicrobial Secretions
• lysozyme
– hydrolyzes bond connecting sugars in
peptidoglycan
• lactoferrin
– secreted by activated macrophages and PMNs
– sequesters iron from plasma
• lactoperoxidase
– produces superoxide radicals

23
Respiratory System
• turbulent air flow deposits microbes onto
mucosal surfaces
• mucociliary blanket
– mucous secretions that traps microbes
– once trapped, microbes transported away from
the lungs (mucociliary escalator)
• can be expelled by coughing or sneezing
• salivation washes microbes to stomach
• alveolar macrophages
– phagocytic cells in alveoli of lungs
24
Gastrointestinal Tract
• stomach • intestines
– gastric acid – shedding of columnar
• intestines epithelial cells
– pancreatic enzymes – secretory IgA
– bile – normal microbiota
– intestinal enzymes – Paneth cells
– peristalsis • produce lysozyme
• produce cryptins

25
Genitourinary Tract
• unfavorable environment
– low pH of urine and vagina
– vagina has lactobacilli
– urea and other toxic metabolic end products in
urine
– hypertonic nature of kidney medulla
• flushing with urine and mucus
• distance barrier of male urethra
26
The Eye
• mucus secreting epithelial membrane

• flushing action of tears
• lysozyme, lactoferrin, and secretory IgA in
tears

27
Chemical Mediators in Nonspecific
(Innate) Resistance
• many already noted (e.g., gastric juices,

lysozyme, urea)
• a variety of defensive chemicals such as
defensins and other polypeptides are also
found in blood, lymph, and other body fluids

28
Bacteriocins
• peptides produced by normal microbiota
• lethal to related species
• produced by gram-positive and gram-
negative cells
• e.g., colicins produced by E. coli
• e.g., lantibiotics produced by gram-positive
bacteria

29
Opsonization
• process in which microbes are coated by

serum components in preparation for
recognition/ingestion by phagocytic cells
– molecules that carry out above are called
opsonins
• some complement proteins are opsonins
– bind to microbial cells, coating them for
phagocyte recognition
30
Figure 32.5

31
Cells of the Immune System
Granulocytes
Mast cells
Monocytes and macrophages
Dendritic cells
Lymphocytes

32
Cells of the Immune System
• each has specialized role in defending host

• leukocytes
– white blood cells
– involved in both specific and nonspecific
immunity
– all arise from pluripotent stem cells

33
Monocytes and Macrophages
• highly phagocytic cells
• make up monocyte-macrophage system
• monocytes
– are mononuclear phagocytic leukocytes
– after circulating for ~8 hours, mature into
macrophages

34
Macrophages
• larger than monocytes, reside in specific

tissues, highly phagocytic
• have a variety of surface receptors
including (pattern recognition receptors)
– recognize pathogen associated molecular
patterns (PAMPs)
• named according to tissue in which they
reside
35
Lymphocytes
• major cells of the immune system
• major populations include T cells, B cells, and
natural killer (NK) cells
• B and T lymphocytes differentiate in bone marrow
from stem cells
– are only activated by binding of specific antigen onto
lymphocyte surface receptors
– after activation replication continues as lymphocytes
circulate and enter lymphoid tissue
– memory cells are activated lymphocytes that do not
immediately replicate, but will do so later in host’s life
when antigen is again present
36
B Lymphocytes
• B cells (B lymphocytes)
–mature in bone marrow
–circulate in blood
–can settle in lymphoid organs
–after maturation and activation are
called plasma cells and produce
antibodies
37
T Lymphocytes (T cells)
• mature in thymus
• can remain in thymus, circulate in blood, or reside in
lymphoid tissue
• like B cells, require antigen binding to surface
receptors for activation and continuation of
replication
• activated T cells differentiate into helper T cells (TH)
and cytotoxic lymphocytes (CTLs)
• secrete cytokines, chemicals that have effects on
other cells, are produced and secreted by activated T
cells
38
39
Phagocytosis
• process by which phagocytic cells (monocytes,
tissue macrophages, dendritic cells, and
neutrophils) recognize, ingest, and kill
extracellular microbes

40
(a) Invading microorganisms are located by
chemotaxis.
The phagocyte cell membrane adheres to the
surface of the microbes.
(b) Ingestion occurs as the phagocyte

surrounds and ingests a microbe or other
foreign substance into a phagosome.
phagolysosome
(c) Digestion occurs as lysozymes surround a

vacuole and release their enzymes into it.
phagosome Enzymes break down the contents of the
phagolysosome
residual
body Produce substances toxic to the microbe.
(d) Any indigestible material remains in the

phagolysosome, which is now called residual
body.
(e) The phagocyte transports the residual

body to the plasma membrane where the
waste is excreted.
Phagocytosis…
• two mechanisms for recognition of microbe

by phagocyte
– opsonin-independent (nonopsonic) recognition
– opsonin-dependent (opsonic) recognition
• phagocytosis can be greatly increased by
opsonization

43
Intracellular Digestion
• after binding, microbes or components can be
internalized and delivered to a lysosome to become
a phagosome
– respiratory burst reactions occur as soon as phagosome
is formed
– toxic oxygen products are produced which can kill
invading microbes
• phagolysosome
• vacuole which results from fusion of phagosome
with lysosome
– presence of toxic chemicals
• e.g., degradative enzymes
• e.g., toxic reactive oxygen intermediates (ROIs)
• e.g., reactive nitrogen intermediates (RNIs)
44
Exocytosis
• process used by neutrophils to expel microbial
fragments after they have been digested
• phagolysosome unites with cell membrane
– results in extracellular release of microbial fragments
• macrophages and dendritic cells undergo process
called antigen presentation
– pass fragments from phagolysosome to endoplasmic
reticulum
– peptide components of fragments combine with
glycoproteins which ultimately become part of cell
membrane
• peptides bound so they are ultimately presented outward
from the cell
45
Specific (Adaptive)
Immunity
Overview of Specific (Adaptive) Immunity
• three major functions

– recognize nonself
– respond to nonself
• effector response
– eliminates or renders foreign material harmless
• anamnestic response
– upon second encounter with same pathogen immune system
mounts a faster and more intense response
– remember nonself

47
Four Characteristics of
Specific Immunity
• discrimination between self and non-self
– adaptive immunity almost always responds selectively to
non-self, producing specific responses against the stimulus
• diversity
– adaptive immunity generates an enormous diversity of
molecules, e.g., antibodies that recognize trillions of different
foreign substances
• specificity
– adaptive immunity can be directed against one specific
pathogen or foreign substance among trillions
• memory
– the adaptive immunity response to a second exposure to a
pathogen is so fast that there is no noticeable pathogenesis
48
Types of Specific Immunity
• humoral immunity
– also called antibody-mediated immunity
– based on antibody activity
• cellular immunity
– also called cell-mediated immunity
– based on action of specific kinds of T
lymphocytes

49
Types of specific immunity
50
Antibodies
• antibody
– immunoglobulin (Ig)
– glycoprotein made by activated B cells (plasma
cells)
– serves as antigen receptor (BCR) on B cell
surface
• found in blood serum, tissue fluids, and
mucosal surfaces of vertebrate animals
– an antibody can recognize and bind antigen
that caused its production
51
Immunoglobulin Structure
• all immunoglobulin molecules have the
same basic structure
– four polypeptide chains
• two identical heavy chains
• two identical light chains
• heavy and light chains connected to each other by
disulfide bonds
– both chains contain two different regions
• constant (C) regions (CL and CH)
• variable (V) regions (VL and VH)
52
A typical structure of an antibody
Figure 33.11

54
Immunoglobulin Function
• Fab binds antigen specifically
– marks antigen for immunological attack
– activates nonspecific defense mechanisms that
can destroy antigen
• e.g., opsonization for enhanced phagocytosis
• Fc mediates binding to:
– host tissue
– various cells of immune system
– first component of complement system
55
Immunoglobulin Classes…
• IgG
– 80% of serum immunoglobulin
– opsonization, neutralization, activates complement
– only Ig that can cross the placenta for natural passive immunity to neonate
• IgD
– part of the B cell receptor complex
– signals B cells to start antibody production
• IgM
– pentamer arranged in pinwheel
– first Ig in all immune responses
– agglutination, activates complement
• IgA, secretory IgA (sIgA)
– monomers and dimers
– secreted across mucosal surfaces
– tears, saliva, breast milk, MALT
– immune exclusion
• IgE
– lowest Ig serum level, elevated in parasitic infection and allergic reactions
– opsonization (binds to receptors on dendritic cells and macrophages)
– mast cells bind Fc portion and are activated to degranulate vasoactive granules
when Fab portion binds allergens
Primary Antibody Response
• several days to weeks lag or latent period
after initial exposure to antigen
– no antibody detectable in blood
• after B cell differentiation into plasma cells,
antibody is secreted
– antibody titer
• is measure of serum antibody concentration
• reciprocal of highest dilution of antiserum that gives
positive reaction
• IgM appears first, followed by IgG
57
Figure 33.14

58
Secondary Antibody Response
• upon secondary exposure to same antigen,

B cells mount a heightened, memory
response
• characterized as having a shorter lag, a
more rapid log phase, longer persistence, a
higher IgG titer and production of
antibodies with a higher affinity for the
antigen

59
Antimicrobial chemotherapy
Chemotherapeutic Agents
• chemical agents used to treat disease
• destroy pathogenic microbes or inhibit
their growth within host
• most are antibiotics
– microbial products or their derivatives that kill
susceptible microbes or inhibit their growth

61
General Characterisitics of Antimicrobial
Drugs
• selective toxicity
– ability of drug to kill or inhibit pathogen while
damaging host as little as possible
• therapeutic dose
– drug level required for clinical treatment
• toxic dose
– drug level at which drug becomes too toxic for
patient (i.e., produces side effects)
• therapeutic index
– ratio of toxic dose to therapeutic dose
62
General Characteristics of
Antimicrobial Drugs…
• side effects – undesirable effects of drugs
on host cells
• narrow-spectrum drugs – attack only a few
different pathogens
• broad-spectrum drugs – attack many
different pathogens
• cidal agent - kills microbes
• static agent - inhibits growth of microbes
63
Antimicrobial Drugs
• inhibitors of cell wall synthesis
• protein synthesis inhibitors
• metabolic antagonists
• nucleic acid synthesis inhibition

64
Inhibitors of Cell Wall Synthesis
• penicillins
– most are 6-aminopenicillanic acid derivatives
and differ in side chain attached to amino
group
– most crucial feature of molecule is the b-
lactam ring
• essential for bioactivity
• many penicillin resistant organisms produce b-
lactamase (penicillinase) which hydrolyzes a bond in
this ring
65
Penicillins…
• mode of action
– blocks the enzyme that catalyzes
transpeptidation (formation of cross-links in
peptidoglycan)
– prevents the synthesis of complete cell walls
leading to lysis of cell
– acts only on growing bacteria that are
synthesizing new peptidoglycan

66
Protein Synthesis Inhibitors
• many antibiotics bind specifically to the
bacterial ribosome
– binding can be to 30S (small) or 50S (large)
ribosomal subunit
• other antibiotics inhibit a step in protein
synthesis
– aminoacyl-tRNA binding
– peptide bond formation
– mRNA reading
– translocation
67
Aminoglycoside Antibiotics
• large family which all contain a cyclohexane
ring and amino sugars
• bind to 30S ribosomal subunit and interfere
with protein synthesis by directly inhibiting
the process and by causing misreading of
the messenger RNA
• resistance and toxicity

68
Nucleic Acid Synthesis Inhibition
• a variety of mechanisms
– block DNA replication
• inhibition of DNA polymerase
• inhibition of DNA helicase
– block transcription
• inhibition of RNA polymerase
• drugs not as selectively toxic as other
antibiotics because bacteria and eukaryotes
do not differ greatly in the way they
synthesize nucleic acids
69
Quinolones
• broad-spectrum, synthetic drugs containing
the 4-quinolone ring
• nalidixic acid was first quinolone to be
synthesized (1962)
• generations of fluoroquinolones produced
now
• act by inhibiting bacterial DNA-gyrase and
topoisomerase II
• broad spectrum, bactericidal, wide range of
infections
70
72
73
Factors Influencing Antimicrobial Drugs
• ability of drug to reach site of infection

• susceptibility of pathogen to drug
• ability of drug to reach concentrations in
body that exceed MIC of pathogen

74
Ability of Drug to Reach Site of
Infection
• depends in part on mode of administration
– oral
• some drugs destroyed by stomach acid
– topical
– parenteral routes
• nonoral routes of administration
• drug can be excluded by blood clots or
necrotic tissue

75
Drug Resistance
• an increasing problem
– once resistance originates in a population it
can be transmitted to other bacteria
– a particular type of resistance mechanism is
not confirmed to a single class of drugs
• microbes in abscesses or biofilms may be
growing slowly and not be susceptible
• resistance mutants arise spontaneously and
are then selected
76
Drug Resistant “Superbug”
• a methicillin-resistant Staphylococcus aureus
(MRSA) that developed resistance to vancomycin
– this new vancomycin-resistant S. aureus (VRSA) was
also resistant to most other antibiotics
– isolated from foot ulcers on a diabetic patient
– Acquired from conjugation with vancomycin-resistant
enterococci (VRE) were isolated from same patient
• these drug resistant organisms are a serious
threat to human health

77
78
Mechanisms of Drug Resistance
• prevent entrance of drug

– drug can’t bind to or penetrate pathogen
• drug efflux (pump drug out of cell)
• inactivation of drug
– chemical modification of drug by pathogen
• modification of target enzyme or organelle
• use of alternative pathways or increased
production of target metabolite
79
80
The Origin and Transmission of Drug Resistance
• immunity genes
– resistance genes that exist in nature to protect
antibiotic producing microbes from their own
antibiotics
• horizontal gene transfer
– transferred immunity genes from antibiotic
producers to non-producing microbes

81
The Origin and Transmission of Drug
Resistance
• resistance genes can be found on
– bacterial chromosomes
– plasmids
– transposons
– integrons
• when found on mobile genetic elements they can be
freely exchanged between bacteria
• chromosomal genes
– resistance results from (rare) spontaneous mutations
which usually result in a change in the drug target
• R plasmids
– resistance plasmids
– can be transferred to other cells by conjugation,
transduction, and transformation
– can carry multiple resistance genes
Overcoming Drug Resistance
• give drug in appropriate concentrations to
destroy susceptible
• use drugs only when necessary
• possible future solutions
– continued development of new drugs
– use of bacteriophages to treat bacterial disease

83
Diseases caused by bacteria
Staphylococcal Diseases
• caused by members of the genus
Staphylococcus
– gram-positive cocci, occurring singly, in pairs,
tetrads, or grape-like clusters
– facultative anaerobes and usually catalase
positive
– normal inhabitants of upper respiratory tract,
skin, intestines, and vagina

85
Staphylococcal Diseases
• caused by members of the genus
Staphylococcus
– gram-positive cocci, occurring singly, in pairs,
tetrads, or grape-like clusters
– normal inhabitants of upper respiratory tract, skin,
intestines, and vagina
• S. aureus – coagulase positive, pathogenic
• S. epidermidis – coagulase negative, less
pathogenic but nosocomial opportunists
• teichoic acid and peptidoglycan contribute to
pathogenicity
Staphlococcal Diseases
• harbored by asymptomatic carriers or

active carriers (have the disease)
– spread by hands, inanimate objects or expelled
by respiratory tract, or through blood
• may produce disease in almost every organ
and tissue
• immune compromised most at risk

87
Figure 38.22

88
Staphylococcal Scalded Skin Syndrome (SSSS)
• treatment, prevention, and control

– isolation and identification based on catalase test,
coagulase test, serology, DNA fingerprinting, and
phage typing
– antibiotic therapy
• many drug-resistant strains
– personal hygiene, food handling, and aseptic
management of lesions

89
Methicillin-Resistant Staphlococcus
aureus (MRSA)
• S. aureus isolates that are resistant to β-

lactam antibiotics (penicillins and
cephalosporins)
• community acquired (CA) – MRSA
– healthy individuals not recently hospitalized
– associated with serious and fatal infection
– may be acquired in health care setting also
90
Diphtheria
• caused by Corynebacterium diphtheriae
– gram-positive
– lysogenized strains produce an exotoxin that inhibits protein
synthesis and is responsible for pathogenesis
– resistant to drying
• airborne transmission by nasopharyngeal secretions
– crowding increases likelihood of transmission
• diagnosis
– observation of pseudomembrane in throat
– bacterial culture
– antitoxin given to neutralized unabsorbed exotoxin in patient’s
tissues
– antibiotic therapy
– active immunization with DPT (diphtheria-pertussis-tetanus) or
acellular DTap vaccine
91
92
Diseases caused by fungi
Direct Contact Diseases
• superficial mycoses
– piedras
• infections of hair shaft
– tineas
• infections involving outer layers of skin, nails, and
hair
– treatment, prevention, and control
• removal of skin scales and infected hairs
• good personal hygiene

95
Direct Contact Diseases…
• cutaneous mycoses
– dermatomycoses, ringworms, or tineas
• different diseases distinguished according to
causative agent and area of body affected
– most common fungal diseases, occurring
worldwide
– diagnosis
• microscopic examination of skin biopsies and
culture on Sabouraud’s glucose agar
– treatment, prevention, and control
• topical ointments and antifungal agents
96
Figure 39.13

97
Direct Contact Diseases…
• examples of cutaneous mycoses

– Tinea capitis – infection of scalp hair
– Tinea pedis – athlete’s foot
– Tinea unguium – infection of the nailbed
– Tinea cruris – jock itch

98
Subcutaneous Mycoses
• caused by saprophytic inhabitants of soil
• introduced in soil-contaminated puncture wounds
• clinical manifestations
– develops slowly over a period of years
– nodules form and ulcerate
– organisms spread along lymphatic channels, producing
more nodules
• diagnosis
– culture and examination of fungus from infected tissue
– antifungal agents and surgical excision

99
Diseases caused by protists
Malaria…
– caused by four species of Plasmodium
– transmitted by bite of an infected female mosquito
– life cycle of plasmodial protists
• sporozoite injected with mosquito bite
• replicates as merozoite in hepatic cells
• released, enters erythrocytes and replicates
• lyses erythrocytes – correlates with fever
– periodic attacks of chills and fever
– anemia can result and the spleen and liver often
hypertrophy
– can cause cerebral malaria in children and nonimmune
individuals
102
Malaria…
• diagnosis
– demonstration of parasites within Wright- or
Giemsa-stained red blood cells and serological
tests
– antimalarial drugs
• resistance has been observed
• chemoprophylaxis for individuals traveling to
endemic areas
– prevention by use of bed netting and
insecticides to control mosquitoes
– new vaccine shows promise
103
104
Diseases caused by virus
Influenza (Flu)
• respiratory system disease caused by influenza virus
– RNA virus; segmented genome
– acquired by inhalation or ingestion of respiratory
secretions
• worst pandemic in 1918 killed ~50 million people
• classified into subtypes based on hemagglutinin (HA) and
neuraminidase (NA), membrane surface glycoproteins
– HA and NA function in viral attachment and virulence
– 16 HA and 9 NA antigenic forms are known; they
recombine to produce HA/NA influenza subtypes

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107
Influenza (Flu)…
– chills, fever, headache, malaise, and general
muscular aches and pains
– recovery usually within 3 to 7 days
– often leads to secondary infections by bacteria
– rapid immunologic tests
– symptomatic/supportive therapy
– inactivated virus vaccine

108
Influenza (Flu)…
• an important feature of the influenza
viruses is the frequency with which changes
in antigenicity occur
– antigenic drift – due to accumulation of
mutations in a strain within a geographic area
– antigenic shift – due to reassortment of
genomes when two different strains of flu
viruses (from humans and animals) infect the
same cell and are incorporated into a single
new capsid

109
Influenza Antigenic Shift
• H5N1 subtype (known as bird flu)
– severe disease and death in humans but low
infection in humans
• H1N1 (swine flu) is current pandemic

110
Acquired Immune Deficiency
Syndrome (AIDS)
• caused by human immunodeficiency virus
(HIV); RNA virus family Retroviridae
– occurs worldwide, causing the great pandemic
in second half twentieth century
– theories on origin of disease
• HIV-1 evolved from chimp virus SIVcpz
• only group M HIV-1 is widespread in U.S.
• HIV-2 is widespread in Africa

111
HIV Life Cycle…
• integrates into host cell’s DNA as a provirus
• can remain latent – asymptomatic
• can direct synthesis of viral RNA 
synthesis of new viral particles
– new virion are assembled and released
through budding and eventual lysis

112
Diagnosis
• viral isolation and culture
• assays for reverse transcriptase activity or
viral antigens
• most commonly done by detection of
specific anti-HIV antibodies in the blood
– routine screening tests use ELISA assays which
have many false positive results which are
retested using Western blot technique
• most sensitive test uses polymerase chain
reaction
113
Treatment
• no cure for AIDS

• treatment directed at reducing viral load,
disease symptoms, and treating disease and
malignancies
• most successful treatment involves a
combination of drugs

114

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Microbial diseases,

detection and control

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• secondary metabolites of fungi

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2. Specific immune response

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• effectiveness impacted by:

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• mucus secreting epithelial membrane

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• many already noted (e.g., gastric juices,

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• process in which microbes are coated by

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• each has specialized role in defending host

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• larger than monocytes, reside in specific

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(b) Ingestion occurs as the phagocyte

(c) Digestion occurs as lysozymes surround a

(d) Any indigestible material remains in the

(e) The phagocyte transports the residual

• two mechanisms for recognition of microbe

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• three major functions

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• upon secondary exposure to same antigen,

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• ability of drug to reach site of infection

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• prevent entrance of drug

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• harbored by asymptomatic carriers or

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• treatment, prevention, and control

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• S. aureus isolates that are resistant to β-