ALAGIE

SURGICAL INFECTIONS AND
TECHNIQUES FOR INFECTION

CONTROL.
1
BY
DR THOMAS AGYEN
KBTH December 11, 2023

OUTLINE
2
 Introduction
 General Principles
 General surgical infections
 Acute and chronic infections
 Venereal disease
 principles of antimicrobial therapy
 Classification surgical operations
 Hospital infections

Introduction
3
Infection was one of the early major obstacles.

Louis Pasteur, Joseph P. Lister and Von
Bergmann,
principles of microbial infection in surgery
were laid down.
Sir Alexander Fleming ,1929 , antibiotic
era ,discovery of penicillin, largely controlled
infections
associated with the upsurge of more virulent
and resistant infections
Establishment of Infection
4
 wound contamination alone does not lead to

infection.
 The dose and resistance
1.The dose and virulence

Generally ,when organisms exceeds 100,000/g of
tissue or per millilitre of exudate.
pH, oxygenation, anaerobiosis, temperature,
protein and carbohydrate nutritional requirements
microbial synergism: e.g. fibrinolysins,
lecithinases, proteases
5
2. The resistance of the patient.

 low enough to permit multiplication of the organisms.
General factors.
 immunological status of the patient: innate immunity +
active or passive immunity
 associated diseases: uncontrolled diabetes, malignancy,
tuberculosis, malnutrition,
 anaemia, chronic renal or liver disease and diseases
affecting
 the immune mechanism –
agranulocytosis, hypogammaglobulinaemia and the
acquired immune deficiency state.
6
local factors
Haematoma formation,
devitalized tissue in the wound provide a
pabulum
de vascularization of the area
presence of foreign bodies blocking the
drainage pathways of the wound.
 Local allergic reactions also open up the
tissues to infection.

General Principles of Diagnosis
7
These incorporate the local and systemic

clinical signs of acute inflammation,
Appropriate laboratory tests.
Systemic manifestations of acute inflammation
include fever, chills, malaise, weakness, nausea
and vomiting;
locally the relevant signs are swelling,
tenderness, heat, discoloration and impairment
of function.
Labs: BF,FBC, SWABS, BIOPSIES

General Surgical Infections
8
The organisms commonly encountered in

surgical infections are
 Staphylococci,
Streptococci,
Pneumococci,
Haemophilus Influenzae
gram negative bacteria.

Staphylococcus aureus
9
Xtics pics
golden yellow
colonies on blood
agar culture plates,
Coagulase positive
Staphylococci are
gram-positive
 rounded organisms

S. aureus
10
 About 50% of healthy people are carriers of staphylococci,
 chiefly in the anterior nares and sometimes on the skin,
 Staphylococcus pyogenes causes
 boils,
 carbuncles,
 styes,
 septic hands,
 breast abscesses
 and osteomyelitis.
 It is the most important cause of wound sepsis and sometimes causes
 deep abscess,
 septicaemia and pyaemia.
 It is also known to cause post- operative bronchopneumonia and
enterocolitis.
 S. albus , coag –ve, gen non patho, low grade inflmn.

Streptococci
11
are gram-positive
organisms
occurring in chains
and are either
 haemolytic or non-
haemolytic.
Alpha- haemolytic,
beta-haemolytic
anaerobic streptococci

Various toxins produced
12
Haemolysin, haemolysing red cells;

Ieucocidin, destroying po1ymorphonuclear
leucocytes;
fibrinolysin, dissolving fibrin;
Erythrogenic toxin, producing erythema of skin;
protease splitting protein',
hyaluronidase, digesting collagen and thus
aiding spread of infection; and
deoxyribonuclease acting on deoxyribonucleic
acid.
13
 Beta-haemolytic streptococci, e.g. Strep. pyogenes are

 the characteristic clear zone of haemolysis, on blood agar
plates. Streptococcus pyogenes
 encountered in the pharynx of 5 to 10% of the
 population and
 spreads by contact, respiratory droplets and
 dust.
 Strains of Lancefield group A are responsible 90 per cent of
human infections.
 It is often responsible for tonsillitis, otitis media, sinusitis,
scarlet fever, celIulitis, erysipelas, puerperal sepsis and
severe wound infection.
 The infection spreads along tissue planes.

14
alpha-haemolytic Streptococcus viridans

implicated in intra-oral infections,
tonsillitis, dental infections
cardiac lesions producing endocardrtis.
 The organisms may also contaminate burns
and chronic ulcers of the skin.,

Coliforms
15
Escherichia coli,
Pseudomonas, and
Proteus organisms.
are gram-negative rods,
widely distributed in nature but are also normal
inhabitants of the large bowel of most
mammals.
In general, those bacilli which do not ferment
lactose are more pathogenic for man;

coliforms
16
Esch. Coli
readily develop resistance to broad spectrum
antibiotics in common use,
elaborate in their capsule a powerful endotoxin
which causes
pyrexia,
rigors
septic shock

coliforms
17
Pseudomonas pyocyanea
widely distributed in nature; they are usually of
low pathogenicity
and are therefore encountered as secondary
invaders in
extensive superficial wounds such as bums.
 Pus produced by these organisms has a
characteristic odour and a bluish green colour.
Pseudomonas pyocyanea produces endotoxin with
actions similar to the endotoxin of Esch. coli

coliforms
18
Proteus vulgaris
gram-negative bacilli found in wounds
secondary invaders.
They also infect the urinary tract
split urea into ammonia and carbon dioxide
thus
turning the urine alkaline with consequent
precipitation of phosphatic deposits.

coliforms
19
E. coli pseudomonas
proteus

Other organisms
20
 Klebsiella
 gram-negative rods usually
 responsible for pneumonic lesions and hepatic abscesses
 may produce wound infections especially after transplantation.
 Haemophilus influenzae
 small gram negative
 bacillus often found in the healthy upper respiratory tract.
 It causes acute epiglottitis, meningitis and bronchitis.
 Pneumococci
 are gram-positive diplococci
 usually encountered as causing lobar pneumonia or
 with other organisms causing bronchopneumonia;
 they may also produce otiits media, sinusitis, meningitis, acute
primary peritonitis in young girls and wound infection.

ACUTE INFECTIONS
21
Cellulitis
Pustules,
Furuncles
Carbuncles
Infective Gangrene

Cellulitis
22
diffuse inflammation of the subcutaneous tissue

From invasion by pyogenic bacteria
spreads along
subcutaneous tissues and fascia1 planes.
Streptococcus pyogenes is the commonest cause;
S. aureus is responsible and
 occasionally symbiosis.
Cellulitis of pelvic origin may be caused by
anaerobes and intestinal organisms.

The portal of entry
23
Invisible puncture,
abrasion,
insect bite,
obvious wounds,
fissures,
ruptured blister,
ulcer or
an operative wound

Signs + Symptoms
24
pain, redness, swelIing and disability.

 Pain is likely to be severe in sites where the
swelling produces tension of anatomically
restrained tissues,
e.g. fingers and back of neck.
In lax tissue such as the face, pain may be
minimal despite gross swelling.
The inflamed area throbs with the distension of
the pulse
aggravated by dependency

25
toxaemia, malaise and prostration.

nature of the bacterial invader rather than the
extent of the lesion.
Streptococcal infection causes the greatest
reaction
Lymphangitis is evident as tender streaks of
discoloured skin.

26
An area of cellulitis may

resolve, leaving apparently normal tissues;
 it may suppurate with discharge of pus or
severe cases brawny oedema may result in
necrosis and tissue replacement by fibrosis.
Gangrene may occasionally supervene.

Cellulitis pics.
27

mgmt
28
Rest, elevation, immobilization of the inflamed

part
application of insulating dressings to prevent
heat loss are comforting.
 Antibiotics such as penicillin IV: are useful in
the early stages
When suppuration occurs, surgical drainage is
indicated.

Cellulitis in Special Situations
29
Scalp cellulitis
Orbit
Ludwig'sAngina
Pharyngo-maxillary Space Infection
phlegmon

Suppuration and Abscess Formation
30
Liquefaction of the dead tissue is produced by

proteolytic enzymes contained in the
polymorphonuclear leucocytes
the mass of bacteria, leucocytes, exudate and
dying tissue residues thus formed is called pus.
A pyogenic membrane of granulation tissue
fluctuancy
Point tenderness

Pustules, Furuncles and Carbuncles
31
 are forms of abscesses peculiar to the skin

 result from infections of hair follicles by Staph. pyogenes.
 blockage of its duct with rise in tension and subsequent
 destruction and stretching of the follicle.
 pustule , The tiny abscess thus formed.
 inflammation may subside with egress of the bead of pus.
 Furuncle =multiple hair follicles =boil
 Carbuncles ;special places as back of neck and trunk
problems
 High fever
 Prostration
 Delirium
 thrombophlebitis

Systemic Effects of Infection
32
Bacteraemia
Septicaemia
Pyaemia

Clinical Manifestations
33
Fever, swings (40" to 42"C),

Chills or rigors
progressive weakness, malaise, apathy mounting to
profound prostration.
GI symptoms of nausea , vomiting are Anorexia
Cerebral manifestations take the form of
listlessness, confusion, acute anxiety state or even
delirium.
Labs reveal significant leucocytosis of10,000 to
20,000 usu left shift, eosinophil disappearance.
Positive blood cultures

Principles of Treatment of Acute Infections
34
Genera1 measures
assessment of the nutritional and
immunological status of the patient
evaluation and management of intercurrent
diseases e.g. DM, CKD, malnutrition, etc
A good general standard of hygiene and
nursing care need to be maintained in all cases
bactericidal broad spectrum antibiotic is
administered until sensitivities known.

35
Local measures
Rest, ensuring adequate immobilization
Elevation
Surgery, strictly avoid in cellulitic +
lymphangitic stages.
Closely monitor for abscess demarcation then
adequate drainage

Infective Gangrene
36
death of large sections of tissue with

superimposed putrefaction
caused by the action of microbial enzymes or
thrombosis of nutrient blood vessels serving
the area.
Classified by causative bacteria as
 Aerobic / Anaerobic
 Monobacterial / multiple bact.

Aerobic Gangrene
37
The causative organisms are highly virulent strains of

Strep. Haemolyticus
often occurring in epidemic forms such as the classic
hospital gangrene.
Improvements in patient care and antibiotic therapy
have virtually eliminated
Tx requires large doses of intravenous penicillin
(erythromycin in penicillin sensitive individuals).
Wide debridement of all necrotic tissues
Scalded skin syndrome…… Staph. aureus.

Burn wound necrosis……… P. aruginosa

Synergistic Gangrene
38
symbiotic infections from two or more bacterial

species,
the resultant lesion is far more fulminant than
the regular lesion usually attributable to either
individual pathogen.
Meleney's Gangrene or Cellulitis with the
anaerobe Peptostreptococcus and the common
aerobe Staph. aureus.

Other Synergistic Gangrene
39
 i) ulcerative gingivitis
 Fusiformis bacillus and a spirochete
 ii) cancrum oris, or noma
 Several sets of gram-positive cocci and bacteroides
Melaninogenicus.
 iii) necrotizing fasciitis
 Combinations of coliforms, staphylococci, anaerobic
streptococci, peptostreptococci and Bacteroides species
infecting subcutaneous tissues
 iv) Fournier's gangrene
 Mixed aerobic-anaerobic organisms (including
Staphylococcus, micro-aerophilic Haemolytic streptococcus,
E. coli, Fusobacterium and Cl. Welchi)affecting the scrotum.

ACUTE SPECIFIC INFECTIONS
40
tetanus
gas gangrene
erysipelas
anthrax
rabies

TETANUS
41
monobacterial infection in many African and

other tropical countries
Worldwide distrubution
Clostridium tetani…. causative agent
an obligatory anaerobic gram-positive bacillus
with characteristic terminal spores, giving a
drumstick appearance

Tetanus
42
 monobacterial infection
in many African and
other tropical countries
 Worldwide distrubution
 Clostridium tetani….
causative agent
 an obligatory anaerobic
gram-positive bacillus
with characteristic
terminal spores, giving
a drumstick
appearance
Tetanus
43
The organism-itself does not damage tissues.

It produces an exotoxin tetanospasmin
Tetanus is a wound infection
 contaminated with soil especially in
agricultural fields.
Especially deep puncture wounds with necrotic
and pyogenic bact.
pyogenic bacteria creates the anaerobic
conditions necessary for the growth of the
organism.
Tetanospasmin actions
44
 disturbance of acetylcholine/cholinesterase
balance
peripheral motor end plates leading
continuous excess of acetylcholine remains,
producing clinically a sustained state of muscle
spasm.
extreme hyperexcitability of motor neurones

anterior horn cells which can result in
explosive and widespread reflex spasm of muscle

Clinical features
45
Incubation period -1 wk to 1 month

Shorter incubation period = worse prognoses
A better prognostic index is the period of onset ie 1st
symptom to 1st reflex spasm
Prodromal period 12 to 24 hrs
(lockjaw or trismus
Dysphagia
Sardonic smile
Opisthotonus
fixed and staring.
headaches, restlessness,
DEATH due to pneumonia / respiratory failure
Treatment /Prophylaxis
46
 Treatment is curative only when instituted early

 prophylactic measures
 immunization.
 Active ~ more effective, delayed
 Passive ~ less effective , immediate, assoc. anaphylaxis
Day 1st , 4th and 7th .. Active immunity develops in 28

day
 in practice, 0.5ml of toxoid and 250 units of human anti-

tetanus serum (ATS) are given subcutaneously.

Treatment
47
neutralizing circulating toxins,

 removing the source of infection,
controlling convulsions or tonic rigidity
Preventing complications or dealing promptly
Isolation of pt. quietness and comfort
Proper wound management
Human immune serum in doses of 500 units
daily IM( 3K -6k)
Horse / bovine sera may be used.

Treatment
48
Mild Cases: rigidity only
 Sedation
The Seriously ill. Rigidity +reflex spasm

+dysphagia
 NG tube, tracheostomy/ ET tube for IPPV
Dangerously ill . major cyanotic convulsive attacks.

 Control spasm , prevent convulsion,
 phenobarbitone, chlorpromazine, diazepam, rectal

paraldehyde
 Nondepolarizing muscle relaxants eg tubocurarine.

Treatment
49
Nutrition
Antibiotics; penicillins. Erythromycin
Eye protection
Despite advancements, death rate remains 15 %
pts die of not the toxin but its effects and
PM reveals association with sympthetic
overactivity

GAS GANGRENE
50
A contributory cause of death in accident cases

The causative organisms fall into two groups
Saccharolytic
 (Cl. welchii or C1. perfringens. Cl. novy,
C1. oedematiens, CI. septicum
Proteolytic
 (Cl. Sporogenes and C1. haemolyticus).

Gas Gangrene
51
organisms are obligative anaerobes with

subterminal spores
producing several lethal toxins
lecithinase (alpha toxin), most powerful,
severe toxaemia with hypotension,
tachycardia,
renal tubular necrosis,
 haemolysis and
cardiovascular collapse

The anaerobes are introduced into the wound from
52
faecally contaminated clothes
thighs and buttocks are particularly prone
Excessive hemorrhage and the use of a tourniquet
are predisposing causes
Concomitant aerobic organisms provides the
growth and metabolic requirement for CL. Welchii
Gross muscle damage and retained foreign bodies
Types
; Clostridium welchii
cellulitis
 Clostridial myonecrosis
Treatment
53
Operative excission
Wound irrigation and packing
Antibiotics usu. Penicillin in massive doses
Gas gangrene serum
Hyperbaric oxygen
DDX
Streptococal myositis

ERYSIPELAS
54
Cutaneous infection with strep. Pyogenes

Mostly affecting lymphatics
Now uncommon due ATBs use.
Invassion is through skin fissures
Mostly affecting face
irritable, stiff, and symptoms of toxaemia rapidly
supervene
oedematous tender raised swelling
appears at the site and begins to spread.
Pain and tenderness
border of the lesion is sharply defined
erysipelas
55

outcome
56
Resolution with some superficial desquamation

Fibrosis of lymphatics and nodes
Penicillin dramatically change prognoses
1 – 2 mega units 6 hourly

ANTHRAX
57
Bacillus anthracis,
a gram-positive
spore-bearing aerobic organism.
It frequently inhabits the wool of various
animals such as cattle, sheep, horses, hogs,
rabbits and pigs and
infection may be acquired from handling
the wool or hides from these animals
Seen among pastoral communities

The disease shows a predilection for the skin,
the respiratory tract and the intestines
58
 three forms
cutaneous lesion
pulmonary form
intestinal form
malignant pustule, resembles carbuncle
fever with rigors, severe weakness, tachycardia
and a cough productive of haemorrhagic sputum
indicating rapidly worsening pulmonary oedema.
 Death occurs in 3-5 days
TX is with Penicillin

59

RABIES
60
An acute, central nervous system infection,

characterized by CNS irritation, followed by
paralysis and death.
 caused a Neurotropic lyssa virus, member of
the Rhabdovirus family.
Transmitted through the bite of a rabid
animal ,mostly dogs
cats, wolves, bats, badgers, skunks, squirrels,
raccoons, horses and cattle

Rabies
61
In a dog bite case , observing the dog for 2 wks

for Symptoms of rabies;
acute restlessness
drooping jaw, profuse salivation
aggressive unprovoked attempts to bite
Negri bodies in dog’s brain confirms diag.

Clinical features
62
 The incubation period Generally 20 days to 2 months.

 determined by several factors:
 • site of the bite wound
• proximity to the CNS
• severity of the bite
• type of virus
• quantity of virus injected into the site
• age of the patient
• immune status of the host
 prodromal period of intense restlessness,
 paraesthesia and hyperaesthesia.
 Pain at the site of the bite

Clinical features
63
 Hydrophobia ( dysphagia) 17 to 80 % of cases

 Muscle spasm and convulsions result from the slightest stimuli
 Generalized paralysis and death two days is inevitable
 Rabies is usually 100% fatal if untreated
 Lab results may indicate:

• Elevated white blood count
• Increased number of polymorphonuclear cells
• Increased number of monoculear cells
• Elevated levels of urinary, acetone, and protein.
• Abnormal number of cells in the cerebrospinal fluid
glucose, acetone,and protein.
• Abnormal number of cells in the erebrospinal fluid

Treatment
64
Prophylaxis with human diploid cell vaccine

(HDCV) in suspected cases
attenuated virus vaccine
Proper local wound care by debridement and
through irrigation reduces no of cases
Preexposure prophylaxis for vet. Workers
Preventive measure - registering, licensing and

vaccinating all dogs.

CHRONIC INFECTIONS
65
Tuberculosis
Actinomycosis
Yaws

TUBERCULOSIS
66
Tuberculosis afflicts a third of the world's

population
in 1995 there were about 9 million new cases of
TB with 3 million deaths.
95% of TB cases and 98% of TB deaths are in the
developing countries.
75% of TB cases in developing countries are in
the economically productive age group (15-50
years)

Tuberculosis
67
 The disease got its name from tubercle which histologically is a

colIection, of lymphocytes and epithelioid cells surrounding the
organism,
 first described by Koch in 1882
 described as acid-fast because it is difficult to decolorize with acid
once stained
 later proceeding to caseation necrosis.
 Two strains of Mycobacterium tuberculosis
 three main routes of primary infection
 direct spread to the lungs
 through the tonsils to the lymph nodes of the neck
 Via the lower iIeum, Peyer's patches
 Tuberculosis of various regions - pulmonary, genitourinary,
bone and joints, peritoneum, etc
Tuberculous Cervical Lymphadenitis
68
entry of the tubercle bacillus through the tonsillar

route….. Upper cervical LN
carrous teeth… submandibular LN
with effective natural immunity, or anti TB drugs
resolution with or without calcification .
But low natural immunity
poor nutritional states
delay of treatment
caseation with cold abscesses formation is the
outcome
collar stud abscess / chronically discharging
sinuses.
Treatment
69
antituberculous therapy
lymph node biopsy confirms diag.
excisional surgery
contra-indications to surgery
 presence of other tuberculous foci e.g. pulmonary or
 gastrointestinal lesions.
 multiple glandular enlargement with
 attendant periadenitis and chronic discharging sinuses
CoIIar stud abscess …aspiration + anti TB drugs

Ulcerated skin excised . Tulle gras dressing +
anti TB
General Management of Tuberculosis
70
 Although anti Tb drugs are available and effective,

there exists programme implementation issues !
 Proper diagnosis
 Case definition ;

i) the site of TB - pulmonary or extra pulmonary
 ii) result of sputum smear-positive or negative
 iii) previous TB treatment
 iv) severity of the TB infection

Categories
71
 Category 1: the sputum smear-positive PTB,

newly diagnosed
• seriously ill patients with severe forms of
TB
 Catcgory 2: relapse, treatment failure, return
after default
 Category 3: sputum smear negative PTB with
limited parenchymal
• involvement and the less severe
• forms of extra pulmonary TB.
 Category 4: Chronic Cases

ANTI TB DRUGS
72
i) Cure the patient of TB with minimum

interference
ii) Prevent death from active disease or its late
effects
iii) Prevent relapse
iv) Prevent emergence of acquired drug
resistance
V) Protect the community from transmission of
the infection

Anti-TB drugs
73

ACTINOMYCOSlS
74
Actinomycosis is a subacute-to-chronic bacterial

infection caused by filamentous, gram-positive, non–
acid-fast, anaerobic-to-microaerophilic bacteria.
 It is characterized by contiguous spread,
suppurative and granulomatous inflammation, and
formation of multiple abscesses and sinus tracts that
may discharge sulfur granules.
The most common clinical forms of actinomycosis
are cervicofacial (ie, lumpy jaw), thoracic, and
abdominal.
In women, pelvic actinomycosis is possible.

Actinomycosis
75
The organism is widely distributed,

occurring in association with grass-like plants
but the pathogenic forms occur as commensals
in the normal mouth.
trauma and presence of carious teeth are
frequent associations.

Actinomycotic lesions
76
xtics pic + potrait
 Firm nodular granulomata

 indurated masses with
indefinite edges.
 locally progressive and
spreads along and
sometimes through fascia1
planes.
 The adjacent tissues
involved but lymph nodes
seldom occurs.
 Chronicity is the hallmark of
actinomycotic infection
Forms of actinomycosis
77
 Cervicofacial actinomycosis (ie, lumpy jaw)
 dental manipulation or trauma to the mouth
 poor oral hygiene, dental caries,
 periodontal disease; may arise following local tissue damage caused

by neoplasm or by osteonecrosis of the jaw or maxilla
 Thoracic actinomycosis
 History of aspiration
 Dry or productive cough, occasionally blood-streaked sputum,
shortness of breath, chest pain
 Abdominal actinomycosis
 History of abdominal surgery, perforated viscus, mesenteric vascular
insufficiency, or ingestion of foreign bodies
 Pelvic actinomycosis
 History of IUCD
 Lower abdominal discomfort, abnormal vaginal bleeding or
KBTH discharge December 11, 2023
Work up
78
preliminary diagnosis of actinomycosis also can

be made by examining sulfur granules
CBC count: Anemia and mild leukocytosis are
common.
Erythrocyte sedimentation rate (ESR) and C-
reactive protein (CRP) levels are often elevated.
Chemistry results usually are normal, with the
exception of a frequently elevated alkaline
phosphatase level in hepatic actinomycosis.
Organism cultures

Treatment
79
eradication of the sources of the organism

Penicillin
surgical deroofing of persistent sinuses
diagnostic laparotomy abd. Masses.

YAWS (FRAMBOESIA
80
contagious inoculable disease

Spirochaete Treponema pertenue
Treponema pertenue which is morphologically
and antigenically indistinguishable from
Treponema pallidum.
chronic infectious disease that occurs mainly in
warm humid regions
T. pertenue penetrates the skin
In most cases, T. pertenue is transmitted from
person to person
Yaws
81
starts as a single lesion that becomes slightly

elevated, develops a crust that is shed, leaving a
base that resembles the texture of a raspberry or
strawberry.
This primary lesion is termed the mother yaw (also
termed buba, buba madre, or primary frambesioma).
Secondary lesions, termed daughter yaws, develop in
about six to 16 weeks after the primary lesion.
Almost all cases of yaws begin in children under 15
years of age, with the peak incidence in 6-10-year-
old children

Clinical features
82
 primary yaws
 The primary lesion is usually extragenital
 leg is the site of predilection
 incubation period 3 to 4 wks
 initial lesion is painless , burst, covered with secretion
or scab..,. Mother yaws. Assoc with mild malaise with
arthralgia.
 Rarely severe reaction is provoked with high pyrexia
bone and joint pains and gastro-intestinal disturbance
which in the infant takes the form of diarrhoea.
 The regional lymph nodes are usually enlarged

Clinical features
83
2nd yaws Secondary yaws

Constitutional symptoms dissapear
The rashes of the secondary stage appear
Maculopapular rashes. symmetrical
distribution on the body
lesion heal leaving pigmented spots.
3rd yaws Tertiary yaws

Formation indolent ulcers which persist for
years
spread circumferentially giving rise to much
.--
scarring and disfigurement.

Clinical features
84
Hand lesions: A scaly dermatitis of the palms

may develop and persist For many years
Dactylitis with swelling of the phalanges,
paronychia and nail atrophy
Foot lesions: cause pain
Head and face lesions: Destructive ulcerating
lesions (gangosa) may involve the hard and soft
palate, nasal cartilages and bones.
Bone lesions take the form of periosritis
Periostitis shows as painful periosteal nodes
Bone deformity and risk of patho. Fracture.
Investigations
85
 RPR or rapid plasma reagent test,
 VDRL test or venereal disease research laboratorytest,

 TPHA or Treponema pallidum hemagglutination test,
 FTA-ABS or fluorescent treponema antibody
absorption),
 (dark-field) Special examination under the microscope
Gram stain organisms are considered to be

Gram-negative poorly stained
silver stain or electron microscopy by researchers

Investigation + Treatment
86
Investigations Treatment
 RPR rapid plasma reagent test,

Penicillin
 VDRL
venereal disease research laboratorytest, anti- treponemal
 TPHA Treponema pallidum
hemagglutination test, agents - salvarsan,
 FTA-ABS fluorescent treponema
antibody absorption), bismuth
preparations
 (dark-field) Special examination under
the microscope
 Gram stain
 organisms are considered to be Gram-
negative poorly stained
 silver stain or electron microscopy by

researchers

VENEREAL DISEASES
87
gonorrhoea,
syphilis
Lymphogranuloma venereum.
The Acquired lmmunne Deficiency
Syndrome(AIDS)

GONORRHOEA
88
is a common sexually transmitted infection

caused by the bacterium Neisseria gonorrhoeae
.
gram-negative reniform, in large numbers
inside the pus cells
diagnosis of chronic cases is of particularly
difficulty
disease shows important differences in its
manifestations in the male from the female

Male Patient
89
Acute Phase: The incubation is about 2 to 10

days
irritation and congestion of the external
urethral meatus.
 A sticky mucoid urethral discharge
Onset of scalding micturition indicates that
anterior urethritis

Local CompIications
90
Anterior Urethra: Folliculitis from infection of Littre‘s

glands (Littritis)
painful perineal swelling. (Cowperitis)
Chordee
Posterior Urethra;
late in gonorrhoea, instrumentation during treatment
precipitates it.
mounting frequency, urgency .
terminal haematuria,
a dull ache in the perineum
the onset of painful nocturnal erections.

91
two glasses urine test differentiates ant. and post.

urethra involvement
infection from the posterior urethra to prostate and
seminal vesicle
Constitutional symptoms of headaches, fever,
generalized aches and pains assoc spread.
Acute sharp pain on defaecation is not uncommon
frequent painful emissions of purulent blood
stained semen.
Chronic prostatitis and vesiculitis are a common
cause of persistent discharge

Complications
92
Stricture formation PID, pyosalpinx,

gonorrheal warts tubo-ovarian abscess
joint infections, Vulvovaginitis
fibrositis, Gonococcal
iridocyclitis and Opthalmia

Gonococca proctitis
conjunctivitis.
Endometrial
Occasionally
involvement
endocarditis
Treatment
93
Penicillin…… high resistance

Cefixime, tetracycline or ofloxacin
advised against sexual activity
Contacts should be traced, examined and
treated
AIl treated patients need to be followed up

ANTIMICROBIAL THERAPY
94
Antimicrobial drugs are chemical agents

Two main types
 synthetic compounds
 products of microbes

General principles
95
antimicrobial agents are adjuncts and not

substitutes
timing of surgical intervention
effective in the early cellulitic and hyperaemic
stages of infection
most effective agent or combination of agents
must be used and in suffcient doses, and periods
Antibiotics usually
 Bactericidal (penicillins and cephalosporins)
 Bacteriostatic (chloramphenicol, erythromycin)

General principles
96
avoid development of side-effects of

antimicrobial treatment.
Correct any physiological deficiencies
 anaemia, dehydration,
 hyperglycaemia, hypoproteinaemia
antibacterial agents are more effective in
controlling established infections than they are
in preventing them

97
1. Clean operations - no bacteriologically colonized

viscus is opened e. g. herniorrhaphy
2. Clean contaminated - bacteriologically colonized
 viscus is opened but contamination is
minimal – inflamed appendicectomy .
3. Contaminated - there is inflammation of a
colonized viscus but no suppuration e.g.
acute appendicitis.
4. Dirty - frank pus or perforation of a viscus.

Prophylactic use of antibiotics
98
significant reduction of infection

GIT most surgeries are classified as clean-
contaminated
Open wounds
Compound fractures
Burns
Cardiac surgery

Selection of antimicrobial agents
99
Broad spectrum ATB , effective in a particular

case
Considering the clinical characteristics
Crystalline penicillin….cellulitis… strep.
Cloxacillin… carbuncle….staph
Cefuroxime + metronidazole….mixed
infections …. Perforated appendix
Clinical judgement is most important for 2nd
invaders obscure sensitivity results

HOSPITAL INFECTIONS
10
0
Nosocomial infection
Greek NOSOKOMEION meaning “hospital
develops in the patients after more than 48 hours of
hospitalization. If less than 48 hrs+ community
acquired
1. Infection can be acquired as cross-infection from
the other patients, hospital staff and visitors
2. Hospital environment
3. Self infection (autoinfection ) from microbes that
are carried by the patient himself on admission to
the hospital
Nosocomial infection
10
1
High risk areas in the
Patient factors
hospital
These areas in the  Extreme age

hospital carry a greater  Primary ailments
risk: complicated by other
Nurseries associated diseases
 immunosuppressive drugs
Intensive care unit
 Indiscriminate use of
Dialysis unit antibiotics and steroids
Organ transplant unit  Longer patient exposure
Burns unit through complicated and
lengthy operative
Operation theatres
procedures.
Delivery rooms
Nosocomial infection
10
2
 Staphylococci are environmental multipliers
 Strains 80, 81 and 77 have epidemic potentials and
virulent drug resistant infections
 Streptococcus is more frequently in the throat but
when in the nasal carrier is more dangerous
 Close personal contact is more important the transfer
of strept. than staph.
 Intestinal organisms, E. coli, proteus and obligate
anaerobes e.g. bacteroides fragilis occur by
autoinfection
 Pseudomonas infection is by cross infection
 Tetanus and gas gangrene by faulty sterilization
Methods of Preventing Hospital Infections
10
3
1 Removal of the  Theatre Design

 theatre suite, Sterilization An
sources and adequate ventilation system,
reservoirs of  bedding brought from the
wards,
infection.  Masks should be well
2. Blocking the designed and well worn,
team members, spectators .
routes of transfer to
the patient.  Surgical wards
 Dressings
3. Increasing the
 Isolation
patient's resistance.  Highly infectious
 reduced resistance

Prevention
10
4
Theatre Design
theatre suite, Sterilization An adequate
ventilation system,
 bedding brought from the wards,
 Masks should be well designed and well worn,

team members, spectators .
Surgical wards
Dressings
Isolation
 Highly infectious
 reduced resistance
What to do in event of infection
10
5
It is important to isolate the organism and type
it,
The clinical features of the infective lesion may
throw light on the source:
specimens should be taken from the anterior
nares and throat
staff in theatre and the wards
Samples taken from the floors, objects in the
theatre, wards and air conditioning plant.

10
6
THANK YOU

ALAGIE

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SURGICAL INFECTIONS AND

TECHNIQUES FOR INFECTION

KBTH December 11, 2023

KBTH December 11, 2023

Infection was one of the early major obstacles.

 wound contamination alone does not lead to

1.The dose and virulence

2. The resistance of the patient.

KBTH December 11, 2023

These incorporate the local and systemic

KBTH December 11, 2023

The organisms commonly encountered in

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

Haemolysin, haemolysing red cells;

 Beta-haemolytic streptococci, e.g. Strep. pyogenes are

KBTH December 11, 2023

alpha-haemolytic Streptococcus viridans

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

diffuse inflammation of the subcutaneous tissue

KBTH December 11, 2023

KBTH December 11, 2023

pain, redness, swelIing and disability.

KBTH December 11, 2023

toxaemia, malaise and prostration.

KBTH December 11, 2023

An area of cellulitis may

KBTH December 11, 2023

KBTH December 11, 2023

Rest, elevation, immobilization of the inflamed

KBTH December 11, 2023

KBTH December 11, 2023

Liquefaction of the dead tissue is produced by

KBTH December 11, 2023

 are forms of abscesses peculiar to the skin

KBTH December 11, 2023

KBTH December 11, 2023

Fever, swings (40" to 42"C),

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

death of large sections of tissue with

KBTH December 11, 2023

The causative organisms are highly virulent strains of

Scalded skin syndrome…… Staph. aureus.

KBTH December 11, 2023

symbiotic infections from two or more bacterial

KBTH December 11, 2023

KBTH December 11, 2023

KBTH December 11, 2023

monobacterial infection in many African and

KBTH December 11, 2023

The organism-itself does not damage tissues.

extreme hyperexcitability of motor neurones

KBTH December 11, 2023