CHAPTER 3 PART 2

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Last updated 12:30 PM on 10/5/23
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161 Terms

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Clinical Findings for Streptococcus pyogenes

  • TONSILLOPHARYNGITIS

  • SCARLET FEVER

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  • Seasonal occurrence

  • Involves children 5-10 years of age

  • Secondary peak at 12 and 18-20 years of age

TONSILLOPHARYNGITIS

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Sign and Symptoms

  • sudden onset of fever, sore throat, headache, nausea, malaise, pain, and marked tonsillo-pharyngeal erythema

TONSILLOPHARYNGITIS

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Complications:

  • sinusitis, otitis media, pertonsillar and retropharyngeal abscess, acute rheumatic fever, and acute glomerulonephritis

TONSILLOPHARYNGITIS

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Diagnosis for TONSILLOPHARYNGITIS

Culture of specimen (swab)

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Treatment for TONSILLOPHARYNGITIS

  • self- limited

  • DOC: PENICILLIN

  • ALT.: ERYTHROMYCIN or CLINDAMYCIN

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Occurs in association with streptococcal pharyngitis

Scarlet Fever

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Sign and Symptoms:

  • pinkish-red rash on the skin

  • spotted strawberry-like appearance of the tongue

  • skin peels off similar to sunburn (as the disease progresses)

Scarlet Fever

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Treatment or DOC for Scarlet Fever

PENICILLIN G

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  • Pneumococci

  • Gram (+),

  • encapsulated,

  • lancet-shaped diplococci

  • Alpha-hemolytic (causes partial hemolysis)

  • Normal inhabitants of the URT;

  • transient flora of the nasopharynx

Streptococcus pneumoniae

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the virulence factor of Streptococcus pneumoniae

Capsule (anti-phagocytic)

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Mode of Transmission:

  • Droplet respiratory secretions

  • Nasopharyngeal carriers (10% cases)

Streptococcus pneumoniae

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clinical findings for Streptococcus pneumoniae

  • Chronic cardio-pulmonary disease

  • Otitis media ( middle ear)

  • Sinusitis (sinuses)

  • Mastoid

  • Meninges

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  • follows URT infections

  • Begins with abrupt onset of fever and chills, cough and pleuritic chest pain

  • Sputum is RED or BROWN (“rusty”) in color

Chronic cardio-pulmonary disease

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Laboratory Diagnosis for Streptococcus pneumoniae

  • Gram’s stain

  • Microscopic examination (sputum)

  • Capsular swelling test (Quellung Reaction)

  • Optochin sensitivity

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Treatment and prevention for Streptococcus pneumoniae

  • DOC: PENICILLIN G

  • Alt.: CEFTIZOXIME and VANCOMYCIN

  • Prevention: PNEUMOCOCCAL CONJUGATE VACCINE

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it is also called as “blood-loving”

Haemophilus

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  • Haemophilus – “blood-loving”

  • Found on the mucous membranes of the URT

  • Most infections occur in children 6 months-6 years

Haemophilus infuenzae

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the virulent factor of Haemophilus influenzae and the most virulent

  • Capsule (anti-phagocytic)

  • H. influenzae type b (encapsulated strain)

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Mode of Transmission for Haemophilus influenzae

it enters the body through the URT

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Clinical findings of Haemophilus influenzae

  • Sinusitis and Otitis media (2nd to Pneumococci)

  • Epiglottidis (exclusively caused by H. influenzae)

  • Meningitis (SSx: Fever, Headache, Stiff neck along with drowsiness)

  • Bronchitis and Pneumonia (commonly seen in elderly adults with chronic respiratory disease)

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Laboratory Diagnosis for Haemophilus influenzae

  • Microscopic Examination

    SPECIMEN (Nasopharyngeal swabs, pus, blood, and spinal fluid)

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Treatment and prevention for Haemophilus influenzae

  • DOC: AMPICILLIN (non beta-lactamase producing strains)

  • Newer Cephalosporins (all strains)

  • Prevention: H. influenzae type b conjugate vaccine (Hib vaccine) to children

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  • Smallest free-living organisms that can self-replicate in laboratory media

  • Produces tiny colonies on special agar that have a "fried egg" appearance

  • Cell wall-less organism (cell membrane = sterol)

  • Part of mouth’s normal flora

Mycoplasma pneumoniae

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mode of transmission for Mycoplasma pneumoniae

person-to-person (infected respiratory secretions)

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Clinical findings for Mycoplasma pneumoniae

  • Atypical or Walking Pneumoniae

    ☆ Asymptomatic carriers

    ☆ Tracheobronchitis with low grade fever, pharyngitis, malaise and non-productive cough

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Laboratory Diagnosis for Mycoplasma pneumoniae

Serologic Testing

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Treatment and prevention for Mycoplasma pneumoniae

  • DOC: MACROLIDE or TETRACYCLINE

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  • An opportunistic pathogen (community-acquired/nosocomial infections)

    ☆ Elderly patients

    ☆ Diabetics

    ☆ Alcoholics

    ☆ Chronic respiratory tract

  • Frequently found in the large-intestine

  • Found also in soil and water

  • Very large capsule (anti-phagocytic)

Klebsiella pneumoniae

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Clinical findings for Klebsiella pneumoniae

  • Lobar Pneumonia – thick, bloody sputum (“currant jelly”)

  • Necrosis and abscess formation are common

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Laboratory Diagnosis for Klebsiella pneumoniae

  • Differential Media: MacConkey’s Agar and EMB

  • Biochemical Tests

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Treatment and prevention for Klebsiella pneumoniae

  • Highly resistant to antimicrobial drugs

  • DOC: Sensitivity Testing

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  • Gram (-) rods

  • It can survive inside macrophages and alveolar cells

Legionella pneumophila

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what is the virulence factor of Legionella pnuemophila

LPS

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mode of transmission for Legionella pneumophila

  • Lakes,

  • streams,

  • air conditioners,

  • and water-cooling towers

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clinical findings for Legionella pneumophila

  • Pontiac Fever

  • Legionnaire's Disease (Legionellosis)

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  • A mild flu-like form of infection

  • Does not result in pneumonia

  • Abrupt but resolves completely in < a week

Pontiac Fever

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  • Atypical type of pneumonia

  • Very high fever and severe pneumonia accompanied by mental confusion and non-bloody diarrhea

  • Can be fatal

Legionnaire's Disease (Legionellosis)

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laboratory diagnosis for Legionella pneumophila

  • Dieterle and Warthin-Starry Silver Stains (Silver Impregnation Method)

  • Monoclonal or Polyclonal immunofluorescent

    Antibody Staining

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Treatment and prevention for Legionella pneumophila

  • Macrolides

  • Fluoroquinolones

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  • Small,

  • encapsulated,

  • Gram (-) rod

Bordetella pertussis

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Mode of Transmission for Bordetella pertussis

Airborne droplets ( severe coughing episodes)

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Stages of Whooping Cough ( Pertussis)

  • Catarrhal Stage

  • Paroxysmal Stage

  • Convalescent Stage

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stage of whooping cough where:

  • Most contagious (greatest number of Mos)

  • 1-2 weeks

  • Mild URT infection with non-specific signs and symptoms

Catarrhal Stage

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stage of whooping cough where:

  • 5-20 forceful, hacking coughs with the production of abundant amounts of mucus that ends in a high-pitched indrawn breaths (“whoop noise”)

  • 2-10 weeks

  • Patient may turn cyanotic, the tongue protrudes, the eyes bulge, and neck veins engorge

Paroxysmal Stage

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stage of whooping cough where:

  • Reduction of symptoms leading to recovery

  • Patient is no longer contagious

Convalescent Stage

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complications of Bordetella pertussis

  • Pertussis, like measles, can unmask underlying

    tuberculosis

  • Convulsions may occur due to cerebral anoxia

    during coughing spells

  • Blindness (from hemorrhages into conjunctiva

    during paroxysms)

  • Pneumonia,

  • deafness, and

  • hernias

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Laboratory Diagnosis of Bordetella pertussis

  • Culture of specimens (nasopharyngeal swabs – taken during paroxysmal stage)

    Regan Lowe Charcoal Medium

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Treatment and Prevention of Bordetella pertussis

  • DOC: MACROLIDES (patients and exposed individuals)

  • Supportive care: Oxygen Therapy and Suctioning of mucus

  • Prevention: Acellular Vaccine

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  • Acid-fast,

  • obligately aerobic bacillus

  • Cell Wall - Mycolic Acid

Mycobacterium tuberculosis

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mode of transmission of Mycobacterium tuberculosis

  • Person-to-person (respiratory aerosols)

  • Fomites (utensils and galsswares)

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transmitted through ingestion of contaminated cow’s milk —— GI tuberculosis

M. bovis

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clinical findings of Mycobacterium tuberculosis

Koch's Disease (Tuberculosis)

  • 1° Infection/ Complex

  • 2° Infection/ Reactivation Pulmonary Tuberculosis

  • Disseminated/ Extrapulmonary Tuberculosis

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  • Initial infection in childhood

  • May affect any part of the lungs (most cases – middle and lower lobes)

  • Ghon Complex (Lesion)

  • Asymptomatic (most ptx)

1° Infection/ Complex

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  • Caused by Mos that have survived in the 1° lesion

  • Almost always begins at the apex (highest oxygen tension)

  • S/Sx: fatigability, afternoon rises in temp, weight loss, night sweats, loss of appetite, chronic non-productive cough with or without hemoptysis.

2° Infection/ Reactivation Pulmonary Tuberculosis

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  • Multiple disseminated lesions

  • Initial organs affected – lymph nodes

  • Scrofula – aggregation and ulceration in the lymph nodes

  • Forms: TB meningitis, TB osteomyelitis (Pott’s

    disease), GI TB, Oropharyngeal TB, Renal TB, GU TB, PerIcardial TB

Disseminated/Extrapulmonary Tuberculosis

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Diagnosis for Mycobaterium tuberculosis

  • Acid-Fast Staining of Sputum

    ☆ 2 collections – 0 hr and 1hr

    ☆ Medium: Lowenstein-Jensen

  • Chest X-ray

  • Tuberculin Skin Test (Mantoux – intradermal test)

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treatment and prevention for Mycobacterium tuberculosis

Bacillus Calmette-Guerin (BCG) vaccine

<p><strong>Bacillus Calmette-Guerin (BCG) vaccine</strong></p>
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clinical findings for Bacillus anthracis

ANTHRAX

  • Cutaneous

  • Gastrointestinal

  • Pulmonary/Inhalation Anthrax (Woolsorter’s Disease)

    edema, enlargement of mediastinal lymph nodes (Chest X-ray - widening of the mediastinum), bloody pleural effusion, septic shock, and death

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complications of Bacillus anthracis

  • Hemorrhagic meningitis

  • Hemorrhagic mediastinitis

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treatment for Bacillus anthracis

  • DOC: CIPROFLOXACIN

  • Alt.: DOXYCYCLINE

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Bacterial Infections of the GIT

  • Gastritis

  • Enteritis

  • Colitis

  • Gastroenteritis

  • Hepatitis

  • Dysentery

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how does disease occur in the GIT?

  1. Pharmacologic Action

    • Toxins

  2. Local Inflammation

    • Invasion of the alimentary tract by microbes

  3. Deep Tissue Invasion

    • Spread of the MO to the adjacent tissues

  4. Perforation

    • Normal Flora spills into sterile areas

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  • alter normal intestinal function without lasting damage to their targeted cells

  • Ex: Vibrio cholerae (Cholera toxin–epithelial cells)

Toxins

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  • usually limited to the epithelial layer but may spread to the deeper tissues.

  • Ex: mouth (periodontitis) and intestine (dysentery)

Invasion of the alimentary tract by microbes

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  • enters the bloodstream

  • Ex: Strongyloides stercoralis (burrowing through the intestinal wall called POLYMICROBIAL SEPTICEMIA)

Spread of the MO to the adjacent tissues

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  • invades deep tissues

  • Ex: perforation of the inflamed appendix- peritonitis

Normal Flora spills into sterile areas

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Causative agents of Dental Caries (tooth decay)

  • Streptococcus mutans (primary)

  • Actinomyces

  • Lactobacilli

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prevention of Dental Caries

  • Minimal ingestion of sucrose,

  • Brushing,

  • Flossing,

  • Regular dental visits,

  • use of fluoride, chlorhexidine (mouthwash)

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inflammation and degeneration of structures that support the teeth

Periodontal Disease

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the causative agent of Periodontal Disease

  • Streptococci

  • Actinomycetes

  • Anaerobic Gram (-):

    1. Prevotella

    2. Bacteroides

    3. Fusobacterium nucleatem

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  • Reversible inflammation of the gums

  • Bleeding of the gums while brushing the teeth

Gingivitis

<p><strong>Gingivitis</strong></p>
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<ul><li><p>Severe/chronic gum disease</p></li><li><p> Bone destruction and tooth loss</p></li><li><p> Gums are inflamed and bleed easily</p></li></ul>
  • Severe/chronic gum disease

  • Bone destruction and tooth loss

  • Gums are inflamed and bleed easily

Periodontitis

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<ul><li><p>Serious, pain that prevents normal chewing</p></li><li><p>Halitosis</p></li><li><p><strong>Prevotella intermedia</strong> (primary)</p></li></ul>
  • Serious, pain that prevents normal chewing

  • Halitosis

  • Prevotella intermedia (primary)

Acute Necrotizing Ulcerative Gingivitis / Vincent’s DSE / Trench Mouth

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Virulence Factors:

  • Rapid Motility (penetration of the lining of the stomach)

  • Urease Production (production of large amounts of ammonia from the urea (neutralization of gastric acid))

Helicobacter pylori

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mode of transmission of Helicobacter pylori

  • Ingestion

  • Person-to-person via the saliva

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clinical findings of Helicobacter pylori

  • Gastritis

  • Peptic Ulcer

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laboratory diagnosis for Helicobacter pylori

  • Histologic examination

  • Culture

  • Measurement of antibody levels

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treatment for Helicobacter pylori

  • Triple Therapy

    Proton pump inhibitor ( OMEPRAZOLE) + Macrolide ( CLARITHROMYCIN) + AMOXICILLIN

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  • Similar symptoms occur in several members of a group who share the same meal

  • Onset of symptoms occurs a few hours after food ingestion

Bacterial Enterocolitis ( Food poisoning)

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the 3 mechanisms of Bacterial Enterocolitis ( Food Poisoning)

  1. Ingestion of preformed toxin may be present in contaminated food ( Staphylococcus aureus, Vibrio, and Clostridium perfringens)

  2. Infection by toxigenic organisms

  3. Infection by an enteroinvasive organism

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  • Gram (+) aerobic bacillus

Bacillus cereus

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clinical findings of Bacillus cereus

  1. Emetic Type

  2. Diarrheal Type

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  • incubation period (1-6 hours)

  • nausea, vomiting, abdominal cramps, and occasionally diarrhea

  • self-limited (recovery: 24 hours)

  • source: re-warmed rice and pasta dishes

Emetic Type

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  • incubation period (6-24 hours)

  • profuse diarrhea with abdominal pain and cramps

  • Enterotoxin may be produced in the intestine

  • Source: meat, poultry, and vegetables

Diarrheal Type

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laboratory diagnosis for Bacillus cereus

Isolation of the organism from the suspected food samples followed by culture

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treatment and prevention for Bacillus cereus

  • Fluid and electrolyte replacement

  • Self-limited

  • Preventive Measures:

    1. Preventing contamination by soil

    2. Rice should not be kept warm for long periods

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  • Causes food poisoning with the shortest incubation period (Average: 2 hours)

  • Enterotoxins – produced when the MO grows in food-rich in CHO and CHON

Staphylococcus aureus

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mode of transmission for Staphylococcus aureus

  • Ingestion of contaminated food – salads, custards, milk products, and processed meat

  • Carriers and individuals shedding human lesions

  • Fomites contaminated with human lesions

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clinical findings for Staphylococcus aureus

  • Vomiting and Nausea (more prominent than diarrhea)

  • Toxin – acts on neural receptors in the gut

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laboratory findings for Staphylococcus aureus

Isolation of the organism from the suspected food samples followed by culture

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treatment and prevention for Staphylococcus aureus

  • Self-limited

  • Fluid and electrolyte replacement

  • Preventive Measures:

    1. cleanliness

    2. hygiene

    3. aseptic management of lesions

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mode of transmission for Clostridium perfringens

Ingestion of preformed toxin from food-contaminated soil containing the MO’s spores – meat dishes

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clinical findings for Clostridium perfringens

  • Incubation Period: 9-15 hours

  • Watery diarrhea with abdominal cramps

  • Self-limiting (24 hours)

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treatment and prevention for Clostridium perfringens

  • Fluid and Electrolyte replacement

  • Preventive measure:

    1. adequately cook food before consumption

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  • Marine organism – bacterial gastroenteritis associated with seafood.

  • Curved, Gram (-) coccobacillus

  • Halophilic (requiring 80% NaCl solution for growth)

Vibrio parahaemolyticus

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toxin that can is present in Vibrio parahaemolyticus

Kanagawa hemolysin (enterotoxin similar to the cholera toxin)

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mode of transmission for Vibrio parahaemolyticus

  • Ingestion of raw or undercooked seafood (shellfish – oysters)

  • Philippines - milkfish

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clinical findings for Vibrio parahaemolyticus

  • Mild to severe watery diarrhea, nausea, vomiting, abdominal cramps, and fever

  • Self-limited (3 days)

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laboratory diagnosis of Vibrio parahaemolyticus

Culture (Thiosulfate–citrate–bile salts–sucrose agar) TCBS Agar

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