Bacterial Infections

I.

STAPHYLOCOCCAL INFECTIONS
Staphylococci
Gram (+)
Singly, in pairs, short chains, clusters
Resistant to high salt conc, heat and drying

Classification:
Coagulase (+) S. aureus
Coagulase (-) non-pathogenic (S. epidermidis, S. hemolyticus, S. saphrophyticus)

i.
ii.
iii.
iv.

Staphylococcus aureus
Virulence is mainly d/t production of enzymes and toxins
4 exotoxins that acts on cell membrane:
Alpha toxin causes tissue necrosis, plt. aggregation and injury to leukocytes
Beta hemolysin hemolysis of RBC and degrades sphingomyelin
Delta hemolysin disrupts membranes by a detergent-like action
Leukocidin toxic to phagocytes
Exfoliative toxins A & B
Bullous impetigo (localized)
Staphylococcal Scalded Skin SyndromeSSSS (generalized)
Staphylococcal enterotoxins
Food poisoning
Enterotoxin F
Toxic Shock Syndrome Toxin-1 (TSST-1)
Related to menstruation

EPIDEMIOLOGY
Many neonates and most children and adults become intermittently colonized by S.
aureus by harboring the org. in their nasopharynx, fingernails, clothing, and skin
PATHOGENESIS
Intact skin and mucous membrane serves as barriers to invasion
Breached (trauma/sx)
Org. can gain access to the underlying tissues
Local abscess lesion
i.

ii.
-

Clinical manifestations
Skin and soft tissue infection
impetigo
folliculitis
small furuncles
extensive areas of cellulitis
Bullous impetigo
SSSS or Ritters dse.
Nikolsky sign gentle stroking of apparently healthy skin leads to peeling
LYELLS dse./Toxic Epidermal Necrolysis (TEN)
2 to drug hypersentivity
Respiratory tract
Pneumonia

Empyema, Pneumatocoeles, Pneumothorax, Pyopneumothorax, Bronchopleural

fistula
iii.
Sepsis
iv.
Toxic Shock Syndrome
Potentially fatal condition caused by TSST-1
v.
Food poisoning
Dx
Isolation of org. from skin lesions, abscess cavities, blood, CSF, or other sites of
infection

Gram stain

Culture
Tx
Localized skin infections

Topical (Mupirocin, Bacitracin)

Oral (Co-amoxiclav, Cephalexin)

Serious or invasive infections

Nafcillin/Oxacillin Iv @ 200-400mkd
MRSA (Mithicillin Resistant Staphylococcus aureus)

Vancomycin (DOC)
II.

STREPTOCOCCAL INFECTIONS
Streptococci
Gram (+) cocci in pairs or chains
Facultatively anaerobe
Catalase (-)

i.
ii.
iii.

Classified on the basis of their ability to hemolyze RBC

Beta-hemolytic complete hemolysis
Alpha-hemolytic partial hemolysis
Gamma-hemolytic no hemolysi

i.

ii.

iii.
iv.
girls

weeks

Epidemiology
Group A Streptococci colonized the nasopharynx of 15-20% of normal children
Clinical manifestations
Respiratory tract infections
Tonsillopharyngitis Group A Streptococci
Scarlet fever Strawberry tongue
Skin infections
Impetigo superficial pyoderma
Ecthyma, Cellulitis
Erysipelas an acute, well-demarcated infection of the skin with lymphangitis
Vulvovaginitis frequently caused by Group A beta-hemolytic Strep in prepubertal
Dx
Throat culture pharyngitis
ASO titer -- >166 TODD units in >80% of untreated children with pharyngitis w/in 3-6
following infection
Complications
Early
Local, lymphatic, or hematogenous extension of infection
Late

Acute Rheumatic Fever

Glomerulonephritis
Tx
Penicillin
Macrolides (alternative) for px who have penicillin hypersensitivity

III.
PNEUMOCOCCAL INFECTIONS

Streptococcus pneumoniae (Pneumococcus)

Major cause of lower respiratory tract infection bacteremia and meninigitis in ALL age
groups

Clinical manifestations
Pneumonia MC clinical presentation of the org.
Mortality rates d/t this infection run as high as 35% with no specific serotypes
associated with fatal infections

Dx
Isolation of the org. from the different body tissues
Culture
Latex agglutination test and countercurrent immunoelectrophoresis

Tx
Penicillin
Macrolide alternative
Vaccination for prevention
IV.
MENINGOCOCCAL INFECTION

Neisseria meningitidis (Meningococcus)

Gram (-), biscuit-shaped diplococcus, found only in man
Fastidious, growth is facilitated by incubation on blood, chocolate, Mueller Hinton, or
Trypticase soy agar in 5-10% CO2

Epidemiology
Common in tropical and temperate climates
Transmission is from person to person through respiratory droplets

Pathogenesis
Nasopharynx
Org. penetrates the mucosal surface
Bloodstream
Localizes in various organs

Clinical manifestations
Incubation period: 1-10days
Acute Meningococcemia
Influenza-like illness with fever, malaise, chills, arthralgia, headache, and GI
complaints
Petechial, purpuric or maculopapular lesions may develop w/in hours with subsequent
hypotension, DIC, oliguria, renal failure, and coma
Waterhouse-Friedrichsen Syndrome bleeding into adrenals in septicemia and shock

Dx
(+) blood culture, CSF, skin petechiae

Tx

Penicillin
ALTERNATIVE: Cefotaxime, Ceftriaxone
Prevention
Chemoprophylaxis
Rifampicin 10mg/kg q 12 x 48 hours (DOC)
Ceftriaxone and Ciprofloxacin alternative drugs
Vaccine meningococcal

V.
GONOCOCCAL INFECTIONS

Neisseria gonorrheae
Gram (-) diplococcus with flattened sides
It grows well in chocolate agar medium enhanced by the presence of CO2
A special medium, Thayer-Martin, combines the use of antibiotics to inhibit the
growth of normal flora and non-pathogenic bacteria

Epidemiology
Gonococcal infections occur only in humans
The source of the org. is exudates and secretions of infected mucous surfaces
Transmission occurs mainly through sexual intercourse but oral-genital contact has
also resulted in dse.
Infants acquire the infection during delivery through contact with the cervical and
vaginal mucous membranes
Incubation period: 2-7days

Clinical manifestations
Ophthalmia neonatorium w/c is usually bilateral, with eyelid and conjunctival edema
Newborn arthritis, scalp abscesses
Prepubertal children MC is vaginitis
Urethritis , endocervicitis and PID in sexually active female adolescents

Dx
Gram stain and culture of exudates or secretions from mucous membranes of
involved tissues
Demonstration of intracellular gram (-) diplococci
Treatment

Ophthalmia neonatorum Ceftriaxone at 25-50 mg/kg/dose IV or IM as single dose

Disseminated infections Ceftriaxone 25-50 mg/kg/day extended to 7 days

Alternative: Cefotaxime at 50-100 mg/kg/dose q 12 hours for 7 days

HEMOPHILUS INFLUENZAE INFECTION
Hemophilus influenza

Most common bacterial infection occurring in infants and young children between 2
mos and 3 yrs

Otitis media, acute bacterial meningitis, cellulitis, epiglottis and pneumonia are the
usual clinical presentations in children

Epidemiology:
o
Hemophilus influenzae type B infection is a disease of very young infants
o
Incubation period is less than 10 days
o
Mode of transmission is by direct contact or by inhalation of droplets of secretions
containing the organisms

Pathogenesis:
o
Upper respi tract Adherence of bacteria with fimbriae or pili invasion of the
ciliated respiratory epithelial cells/destruction of the infected cells local inflammatory
response bacteremia


Clinical Manifestations
o
Acute Bacterial Meningitis
o
Pneumonia
o
Otitis Media, sinusitis
o
Epiglottitis
o
Second most common cause of septic arthritis (Staph. Aureus 1st)

Diagnosis
o
Isolation of the organism from the infected body fluids

Gram staining

Culture

Treatment
o
Ampicillin, 2nd and 3rd Cephalosphorins, Chloramphenicol

Prevention:
o
Polysaccharide Conjugated Vaccine
DIPTHERIA
Corynebacterium diptheriae

Characterized by the formation of a pseudomembrane, commonly in the faucial area

and tonsils, and the elaboration of a powerful exotoxin affecting important viscera as the
heart and kidneys, and the peripheral nervous system

Etiology
o
C. diptheriae Gram (+)
o
Organism manufacture an exotoxin responsible for the major pathologic changes

Epidemiology
o
Endemic throughout the world, except in developed countries
o
Philippines cases found throughout the year
o
December through February Higher prevalence
o
Between 2 and 5 years peak incidence
o
Below 6 months rare
o
Transmitted through discharges and secretions from lesions by direct or indirect
contact with patients or carriers, and through various articles including toys and clothing

Pathogenesis
o
The typical pseudomembrane is formed by leukocytes, fibrin, necrotic tissues and
microorganisms, which is adherent to the underlying tissues and leaves a raw bleeding area
when detached
o
Membranes are found nose, nasopharynx, larynx, and other body surfaces
o
Toxin elaborated by organism initiates and contributes to the further growth of the
lesion and the formation of more toxin, which attacks the myocardium, kidneys, liver, cranial
and peripheral nerves producing foci of necrosis and degeneration

Clinical Manifestations
o
I.P 2 days to 1 week
o
Disease is classified on the basis of location of the membrane
o
Low-grade fever, toxaemia with rapid pulse disproportion to fever common features
o
Faucial insidious onset, low-grade fever, malaise, headache, sore throat, and slight
cervical lymphadenopathy
o
Small yellowish white spots appear on the tonsils within 24 hours which coalesce to
form the adherent pseudomembrane
o
Extends to the rest of the fauces nasopharynx
o
Cervical lymph node enlarge further, frustration prominent, rapid, feeble soft pulse
and low BP
o
Dysphagia and noisy breathing, nasal voice and regurgitation of fluids through the
nose due to palatal weakness or paralysis

o
Bull-neck appearance
o
Death occurs from bronchopneumonia or toxic myocarditis
o
Laryngotracheal extension of pharyngeal type, more common in infants
o
Hoarseness with barking cough and noisy breathing followed by inspiratory stridor,
aphonia and marked dyspnea with supraclavicular and suprasternal retraction
o
In severe cases, there is marked prostration and progressive obstruction which leads
to suffocation and cyanosis or cardiac failure and death
o
Nasal occurs mostly during 1st 3 years of life

Benign subacute or chronic

Serous nasal discharge which later becomes bloody and foul-smelling

Unilateral or bilateral

Mild and vague constitutional symptoms

o
Diptheria in the other parts of the body

Usual locations: conjuctivae, umbilical area in the newborn, external genitalia

(females), external auditory canal, wounds and ulcers in the skin
o
Complications:

Bronchopneumonia and respiratory failure-common in laryngeal type and in laryngeal

type and in infants

Cardiac manifestations due to toxic myocarditis 1st 10-14 days

Toxic peripheral neuritis may appear early or late; palate, EOM

Diaphragm, skeletal muscles

Toxic nephritis albuminuria, casts, edema

o
Diagnosis

Early smears and culture

Schick test dermal injection of dilute diphtheria toxin positive in individuals

without immunity
o
Prophylaxis active immunity

DTP immunization program in infancy and childhood

Provides protection for about 10 years

booster given at suitable intervals until adulthood

Moloney test indicates sensitivity to diphtheria toxoid, and should be done in older
children and adults before their toxoid is given to avoid severe reactions

Passive immunity administration of 10,000 units of anti-toxin and lasts for about 3
weeks
o
Treatment:

Isolation, bed rest and maintenance of fluid and electrolyte balance and nutrition

Penicillin (100,000 /kg/day) for 14 days

Erythromycin (40 mg/kg) for 14 days

Early administration of diphtheria antitoxin aimed at neutralizing the toxin present in

the general circulation before it is absorbed by the tissues
o
Treatment of Complications:

Circulatory complication oxygen, digitalis, diuretics and salt-poor diet

Corticosteroids

Plasma or whole blood and vasopressors

Paralysis physical therapy and high doses of vitamin B complex

Dyspnea high moisture atmosphere, intubation, tracheostomy and clearing of

secretions
PERTUSSIS (Whooping cough)

A common and serious infection of the respiratory tract of infants are children

The attacks of paroxysmal cough are often described as bursts of short expiration
followed by a long forced producing a distinct sound called whoop


Clinical Manifestations:
o
Symptomatic illness starts within 1-3 weeks
o
3 stages:

Initial (catarrhal)

Sneezing, runny nose, lacrimation, mild cough and low grade fever

Cough
o
Becomes irritating at night (1-2 weeks)

Middle (Paroxysmal)

Coughing, frequent and severe towards end of 2nd week

Expiratory phase 5x successive forceful cough and end in whoop

o
During cough episode protruding tongue bulging of the eyes, neck vein distention,
cyanosis
o
At the end of the violent cough vomiting, sweat profusely, involuntary urination,
exhausted and lethargic. Epistaxis, periorbital edema, subconjunctival hemorrhages,
petechiae of face and neck, convulsion

Final or Convalescent

Less frequent and milder attacks of paroxysmal cough and a reduction of episodes
vomiting and seizures

Complete recovery after 2-3 weeks

Complications

Pneumonia most common

Death occurs usually among infants and children

Paroxysmal stage forceful coughing may result in rupture of alveoli producing

spontaneous pneumothorax and subarachnoid hemorrhages

Convulsions and come secondary to cerebral anoxia or brain damage following

hemorrhages

Diagnosis

Marked leucocytosis (20-50,000 cells/cumm.)

Increase lymphocytes

Radiology: perihilar infiltrates, air trapping and atelectasis

Best isolated during early stage of illness using nasopharyngeal swabs for culture

Treatment

Erythromycin (50 mg/kg/day)

Other Macrolides (14 days)

Ampicillim (100 mg/kg/day) (14 days)

Supportive therapy: fluids, nutrition, gentle aspiration of thick mucous in infants is

very important

Prevention: active immunization

DPT 3 equal doses given 4-8 weeks apart and a 4th dose (booster) one year later and
another booster after 3-5 years

Exposed children < 7 years old: DPT + Erythromycin

TETANUS

Etiology: Clostridium tetani

o
Motile, gram (+) anaerobic rod that forms terminal pores resembling drumsticks or
tennis rackets
o
Spores are resistant to boiling water and disinfects but destroyed by autoclaving

Epidemiology:
o
Associated with contamination of the umbilical stump, chronic ear infections,
puncture wounds in older children, carious teeth, ear piercing, and pregnancy

Clinical Manifestations
o
3-14 days, incubation period after injury

o
Three Clinical forms

1. Localized tetanus produces pain and continuous rigidity and spasm of muscle in
areas contiguous to the wound which last for weeks without sequelae or may evolve into
generalized tetanus

2. Generalized tetanus most common

Early sign is trismus (lockjaw) with neck muscle stiffness and dysphagia

Risus sardonicus due to spasm of the facial muscle

Opisthotonus persistent spasm of the back muscles

Tetanic seizures sudden burst of tonic contractions of various muscles with flexion
and adduction of the arms clenching of fists and extension of legs

3. Cephalic tetanus

Resulting from head wounds, chronic otitis media or carious teeth and CN VII
dysfunction

It can remain localized or evolve into generalized tetanus

Neonatal Tetanus

Generalized in type and starts as progressive difficulty in sucking and irritability

Diagnosis
o
Based on history and clinical presentation
o
History of absent or incomplete immunization and history of trauma within the 14
days is usual

Complications:
o
Sepsis and bacterial pneumonia

Treatment
o
Aims of therapy:

Neutralize circulating toxin tetanus immune globin

Remove the source of tetanospasmin

Penicillin G, Metronidazole

Wound cleaning and debridement

Provides supportive care

Prevention
o
Tetanus toxoid immunization
o
Infants DPT 3 equal doses given 4-8 weeks apart and a 4th dose (booster) one year
later and another booster after 3-5 years
o
Pregnant women tetanus toxoid 2 doses 4 weeks apart and 2 weeks before dlivery
o
Tetanus immunoglobin
TYPHOID FEVER

Is a general in infection caused by Salmonella typhi, involving primarily the lymphoid

tissues (Peyers patches) of the small instestine

Etiology and Epidemiology

o
Salmonella typhi Gram (-), non-motile and non spore-forming bacillus
o
Antigens 0 (somatic), H(flagellar) and Vi (carbohydrate envelope)
o
8-14 days incubation period
o
Infection contracted from foods like milk, milk products, seafood and shellfish and by
drinking contaminated water
o
Common age group: 16-30 years old

Pathogenesis
o
S. typhi bloodstream Gall Bladder and Upper GIT from upper GIT to Lymph
nodes (peyers pathches necrosis and ulceration), spleen, liver

Clinical Manifestations
o
Fetal Typhoid


Fetus may be infected if pregnant woman contracts typhoid fever fetal death
o
Typhoid in infancy

During the 1st 2 years of life

Resembles septicaemia or gastrointestinal disturbance

Temperature: septic spiking or saw-tooth type of fever lasts for 2 weeks

Diarrhea or constipation, abdominal distention

Rose spots and splenomegaly

o
Typhoid in children (above 2 y.o)

Resemble those seen in adult

Less severe and mortality is low

Initial stage: acute respiratory

Infection, low grade to high grade fever

Relative bradycardia

Abdominal pain with distention and tenderness and splenomegaly

At the end of the 1st week, rose spots appear

Atypical skin manifestations in the form of generalized maculopapular eruptions

resembling dengue, urticarial-like rashes or even petechial are noticed

In the 2nd week, fever is sustained high level and pulse becomes more rapid

Mental turpor, disorientation or delirium may be observed

Abdominal symptoms may become marked

In severe cases symptoms may persist

3rd week complications occur

o
Complications

Intestinal haemorrhage perforation, peritonitis

Hepatitis with jaundice may occur

Pneumonia may result from concomitant Gram (+) infection

Otitis, arthritis, osteomyelitis, nephritis, meningitis, encephalitis or psychosis may be

seen
o
Laboratory

Leucopenia in children

Leukocytosis or normal in infants

2nd week (+) blood culture

2nd week (+) urine culture

3rd week (+) stool culture

Bone marrow culture (+) at any stage

Typhidot

Widal Test not specific

o
Diagnosis

Blood and stool culture for definitive diagnosis

o
Prophylaxis:

Hygiene and public health measures

Immunization
o
Treatment

Chloramphenicol DOC

Ceftriaxone for multi-drug resistant typhoid

Amoxicillin, Ampicillin, Co-trimoxazole, Ciprofloxacin, Azithromycin

Supportive:

Antipyretics

Fluid and Electrolyte balance

Proper nutrition and blood transfusion

SHIGELLOSIS


Acute diarrheal syndrome with bloody or mucoid stools associated with dehydration,
systemic signs of toxicity and neurologic manifestations

Etiology:
o
Shigella slender non-motile gram (-) rods
o
Four serologic groups:

S. dysenteriae

S. flexneri

S. boydii

S. sonnei
o
Spread thru fecal-oral route; contamination, improper handling of food, unhygienic
stool disposal or transmitted by insect vectors
o
Incidence: 1 and 4 y.o. rare before 6 mos.

Pathogenesis
o
Shiga cytotoxin inhibits protein synthesis within the cells diffuse acute colitis
ulceration bloody stool
o
Small intestines not involved in the disease process

Clinical manifestations
o
3-7 days incubation period S. dysenteriae
o
1-3 days others
o
Acute onset of malaise, fever, crampy, abdominal pain followed by watery or pastelike consistency, tenesmus and urgency
o
Within 48 hours stool become bloody or mucoid and small in amount
o
10-45% - seizure, drowsiness, lethargy may occur

Diagnosis
o
Stool culture

Treatment
o
Nalidixic acid
o
Co-trimoxazole
o
Ciprofloxacin
o
Chloramphenicol
o
Supportive

Prevention
o
Good sanitation and hygiene
CHOLERA

One of the most severe diarrheal syndromes characterized by massive loss of fluids
resulting in rapid dehydration and shock

Diarrhea is caused by the in vivo production of enterotoxins which stimulate the

intestinal secretion of fluids and electrolytes

Death from dehydration, acidosis and circulatory collapse in untreated cases

Etiology: Vibrio cholera

o
Gram (-), curved bacillus, highly motile
o
Disease is spread thru fecal contamination of water, milk and other foods
o
Animal vectors are not considered

Pathogenesis and Pathology:

o
V. cholera Enterotoxin (choleragen) binds to a receptor on the surface of the cell
activates intracellular andenylate cyclase cyclic adenosine monophosphate (cAMP)
blocks sodium absorption and promotes excretion of water and chlorides

Clinical Manifestation:
o
2-3 days incubation period
o
Sudden onset of profuse watery diarrhea, severe vomiting and abdominal cramps

o
Stools are whitish to greenish slightly mucoid with any fecal matter, so called ricewater stools and fishy odor
o
Signs of severe dehydration occur rapidly

Laboratory:
o
Hemoconcentration with increase Hgb levels
o
Marked metabolic acidosis and hyperelectrolytemia (decrease K)
o
Increased plasma specific gravity

Diagnosis
o
The clinical features are fairly diagnostic especially in the presence of an epidemic

Complications:
o
Acidosis and shock
o
Hypocalcemia and hypokalemia
o
Renal failure and uremia due to tubular necrosis

Treatment
o
The water and salt lost in cholera stool must be replaced in comparable amount and
concentration
o
Oral rehydration salts
o
Intravenous fluid replacement
o
Tetracycline DOC
o
Co-trimoxazole
E. COLI INFECTIONS

Organisms incriminated in the diarrheas in the newborn and infants especially in

epidemic forms, in sepsis and meningitis of the newborn and in UTI

Diarrheagenic or enteropathic stains

2 categories:
i.
Enterotoxigenic watery, colorless, or greenish, foul, EXPLOSIVE and abundant
ii.
Enteroinvasive bloody mucoid with plenty of cellular elements

E. coli strain (055:K59:H4)

Produces a cytolethal distending toxin to produce gastroenteritis and
encephalopathy, cardiovascular, and hepatocellular dysfxn.

Acute UTI unexplained fever, vomiting or diarrhea

E. coli sepsis in the newborn fever, jaundice, anemia, and diarrhea

PSEUDOMONAS INFECTIONS

Pseudomonas
Gram (-) aerobic rods
Produce dse. in any individual, usually opportunistic and cause dse. in px with burns,
malignancies, immunodeficiency conditions, receiving immunosuppressive therapy or
malnourished

Pseudomonas aeruginosa
Most important
Infective agents in the newborn nursery (prematures), malnourished children,
receiving antibiotics and immunosuppressive drugs, in burns and neurosurgical px
Org. produce vasculitis involving the tunica media blood vessels
thrombotic
infarction
gangrene
Pseudomonas septicemia is
morbidity and mortality

Endocarditis, corneal infection, otitis externa, mastitis, mastoiditis, meningitis,

pneumonia, peritonitis and UTI
Outbreaks of hosp. infection arise from contaminated equipment and solns such as
incubator, O2 humidifying bottles, suction bottles
Dx:
recovery from the blood, CSF, and urine
Tx:
Ceftazidime, Imipenem, Meropinem, Amikacin
ANAEROBIC INFECTIONS

CNS infection anaerobic org. play a role in intracranial infections either as principal
or contributing agents true for brain abscess w/c occurs in px with Chronic Otitis Media,
mastoiditis, sinusitis, or in children with CHD

Oral infections dental abscess or gingivitis

Skin infections found in the sebaceous glands and hair follicles

Lowe respiratory tract infections pneumonia, necrotizing pneumonia and lung

abscess

Abdominal infections peritonitis caused bay appendicitis or GI perforation

Osteomyelitis 50% caused by peptostreptococci; foul odor

Leprosy
Chronic dse. with an insidious onset, transmitted from man to man with protean
manifestations affecting the skin, mucous membranes, nervous tissue eventually producing
physical deformities
Direct transmission in man mainly thru inhalation; neither hereditary or congenital
Pathology and pathogenesis:

Lesions are mainly in the skin, peripheral nerves and mucosa of the upper respiratory
tract

M. leprae proliferative in the Schwann cells of the nerves and produce foamy
degeneration of the axons with marked fibrosis and destruction of normal structure

Leptomatous nodules contain large lipid laden macrophages and giant cells filled
with bacilli (Virchow lepra cells)

Cell Mediated Immunity play a large part in the production of leprosy lesions
Clinical manifestations:

Incubation period: 2-5 yrs or more

Indeterminate lesion initial manifestation :pale, oval or rounded macules, popular

nodules or circinate patches found in the malar area, extremities or buttocks

Lymphadenopathy, anhydrosis, ichthyosis, and limb weakness

Lepromatous

Nodular lesions numerous in the face

Give rise to leonine facies

Diffuse skin infiltrations lead to falling hair and skin atrophy

Ulceration of the nodules and necrosis produce the classical mutilation lesions of
adult leprosy
Dx:

Basis:
i.
Clinical systemic skin or peripheral nerve involvement
ii.
Microbiologic demo the org. in the skin or mucosa
iii.
Histopathologic (+) foamy cells
iv.
Immunologic based on the lepromine test using a (+) or (+) Mitsuda rxn
Tx:
i.
Multi-bacillary leprosy
Rifampicin, Clofaximine, and Dapsone
2-5 yrs

ii.
-

Paucibacillary
Rifampicin and Dapsone
6mos.

Leptospiros
Acute systemic infection that follows contact with blood, urine, tissues or organs of
infected animals
Org. enter thru breaks in the skin or penetrate the mucous membranes including
nasopharynx, conjunctiva or vagina
Etiology:

Rodents most important reservoir

L. pyogenes and L. manilae MC found strains

Pathology

Clinical manifestations:

Acute sx extensive vasculitis from symptomatic to a fatal outcome

3 stages:
i.
Septicemic
4-7 days, fever, headache, myalgia, abdominal pain, and conjunctival suffusion
ii.
Immune or toxic
Leptospiuria is a prevalent affecting renal fxns.
Diminution of fever with rash, conjunctival infections, headache, meningeal
manifestations, aseptic meningitis, iritis or iridocyclitis
Hepatic injury could also be pronounced in some cases producing (Weils syndrome)
iii.
Convalescence
Dx:
i.
Microscopic agglutination test (MAT)
ii.
Complement fixation
iii.
Indirect immunofluorescence
iv.
Counterimmunoelectrophoresis
v.
ELISA
Tx:
i.
Penicillin (DOC)
ii.
Tetracycline alternative
iii.
Supportive

Syphilis
Etiology: Treponema pallidum

Congenital syphilis is acquired from an infected mother via transplacental

transmission of spirochetes most likely in the 3rd trimester

Acquired syphilis is contracted almost always thru sexual contact

Purulent or blood tinge nasal d/c (snuffles) seen in 10% of cases

Hepatomegaly, hyperbilirubinemia, increase liver enzymes, lymphadenopathy,
osteochondritis, thrombocytopenia, leukocytosis frequent
Late congenital syphilis results from the chronic inflammation of bone, teeth and
CNS

Skeletal changes frontal bossing (Olympian brow), anterior bowing of the midportion of the tibia (Saber shin)

Hutchinsons teeth, saddle nose, interstitial keratitis, nerve VIII deafness, and
Cluttons joints
Dx:
Dark field microscopic exam
Direct fluorescent Ab test
Tx: Penicillin G (DOC)
HELICOBACTER PYLORI INFECTION
Etiology:
gram (-) spirally curved microaerophilic bacilli
Clinical manifestations:

Incubation period: unknown

Epigastric pain, N/V, hematemesis

Guaiac (+) stools

Short course some develop duodenal or gastric ulcers

Prolonged infection risk for gastric adenoCA

Dx: Biopsy
Tx: Triple therapy with Amoxicillin or Clarithromycin, Metronidazole, Bismuth
subsalicylate
CHLAMYDIA PNEUMONIAE
Clinical manifestations:

Pneumonia of newborn distinctive, repetitive, staccato cough, afebrile, tachypnea,

rales

Eosinophilia, elevated IgM and IgG

X-ray: hyperinflation

Older children and adolescent c. pneumoniae infections mild atypical or

mycoplasma-like illness