Bacterial infections Diphtheria Pertussis and Enteric fever Dr
Bacterial infections Diphtheria, Pertussis and Enteric fever Dr Mubarak Abdelrahman Assistant Professor Jazan University
Gram negative: Diplococci Bacilli Coccobacilli Gram Positive: Diplococci Chains Clusters Rods & cocobacilli
Diphtheria (Corynebacterium diphtheriae) • An acute toxic infection caused by • Corynebacterium diphtheriae • A gram-positive bacilli.
Epidemiology C. diphtheriae : • An exclusive inhabitant of human mucous membranes and skin. • Spread by airborne respiratory droplets and direct contact. • Can remain viable in dust for 6 months.
Pathogenesis The exotoxin: • Inhibits protein synthesis and causes local tissue necrosis. • In respiratory tract leads to pseudo-membrane. • Absorption can lead to systemic manifestations: e. g. kidney tubule necrosis, thrombocytopenia, cardiomyopathy, demyelination of nerves, . .
Clinical Manifestations The manifestations are influenced by: • The anatomic site of infection. • The immune status of the host. • The production and distribution of the toxin.
Respiratory Tract Diphtheria • Incubation period of 2 -4 days (<7). • Local signs and symptoms of inflammation. • Soft tissue edema + enlarged lymph nodes causes a bull-neck appearance.
A B A: Bull neck B: pseudo membrane C: Skin diphtheria C
Diagnosis • Differential diagnoses: - Epiglottitis. - Exudative pharyngitis caused by Streptococcus pyogenes or Epstein-Barr virus. • Diagnosis: - Helped by the characteristic adherent membrane and relative lack of fever. - Specimens for culture from nose, throat and any other mucocutaneous lesion.
Complications • Respiratory tract obstruction. • Toxic cardiomyopathy In 10 -25% of patients with respiratory diphtheria and is responsible for 50 -60% of deaths. • Toxic Neuropathy acutely or 2 -3 weeks after onset of oropharyngeal inflammation: - Local paralysis: soft palate, pharynx, larynx, . . - Cranial neuropathies: oculomotor paralysis. - Symmetric polyneuropathy.
Treatment • Specific antitoxin: Should be administered on the basis of clinical diagnosis. • The antibiotics (Erythromycin or penicillin) - Stop toxin production. - Treat localized infection. - Prevent transmission of the organism to contacts. • Supportive Care: - Bed rest is essential for ≥ 2 weeks (the period of risk for symptomatic cardiac damage).
Prevention • Protection by immunization with toxoid. • All contacts are: - Closely monitored through the incubation period. - Given Antimicrobial prophylaxis regardless of immunization status. • Asymptomatic carriers also treated.
Pertussis (Bordetella pertussis and Bordetella parapertussis) Pertussis meaning intense cough. Also known as whooping cough. Etiology: by Bordetella organisms: - Gram-negative coccobacilli. - Colonize only ciliated epithelium.
Epidemiology • Pertussis is extremely contagious. • B. pertussis does not survive for prolonged periods in the environment. • Chronic carriage by humans is not documented. • Subclinical infection is around 80%. • Neither natural disease nor vaccination provides complete or lifelong immunity.
Pathogenesis • The exact mechanism of disease remains unknown. • B. pertussis expresses pertussis toxin (PT) and other biologically active substances may be responsible for the local epithelial damage that produces respiratory symptoms and this facilitates absorption of PT.
Clinical Manifestations • Incubation period 3 -12 days. • Classically divided into 3 stages: 1. The catarrhal stage (1 -2 weeks) congestion, rhinorrhea, low-grade fever, sneezing, lacrimation, . . 2. The paroxysmal stage (2 -6 weeks) the cough begins as dry, intermittent, irritative, paroxysmal followed by a loud whoop ± Post-tussive vomiting. 3. The convalescent stage (≥ 2 weeks) the number, severity and duration of episodes diminish.
Clinical Manifestations cont. • Infants <3 months: - No classic stages. - Apnea may be the only symptom. - Cyanosis is common. - Sudden infant death. • In non immunized infants: - Cough and whooping louder and more classic. • Adolescents and previously immunized children: - Mild illness.
On physical examination: • No signs of lower respiratory tract disease. • Can be complicated by secondary pneumonia. • Conjunctival hemorrhage. • Petechiae on the upper body are common.
Diagnosis • A clinical case definition of cough of ≥ 14 days’ duration with at least 1 associated symptom of paroxysms, whoop, or post-tussive vomiting. • Absolute lymphocytosis is characteristic in the catarrhal stage. • Diagnosis confirmed by: 1. Isolation of B. pertussis in nasopharyngeal swab culture (main). 2. Serologic tests: detection of antibodies to B. pertussis.
Complications 1. Apnea. 2. Secondary infections (otitis media, pneumonia, . . ). 3. Physical sequelae of forceful coughing e. g: - conjunctival hemorrhages. - epistaxis. - hemorrhage in the central nervous system. - pneumothorax. - umbilical and inguinal hernias. 4. Bronchiectasis has been reported.
Treatment • Infants <3 months of age with suspected pertussis are always admitted to hospital. • Antibiotics are always given when pertussis is suspected or confirmed. • Macrolides are the preferred agents (erythromycin, Azithromycin) • Isolation of patients and prophylaxis antibiotics to all contacts regardless of age or immunization.
Prevention • Immunization with pertussis vaccine, beginning in infancy with periodic reinforcing doses through adolescence and adulthood.
Enteric Fever (Typhoid Fever) Etiology: Typhoid fever is caused by Salmonella Typhi and S. Paratyph, a gram-negative bacilli.
Epidemiology • In developed countries: <15 cases/100, 000. • In the developing world, estimated rates bet. 100 to 1, 000 cases/100, 000 population. • The highest incidence, complications and hospitalization in children <5 years of age. • Direct or indirect contact with an infected person (sick or chronic carrier) is a prerequisite for infection.
Pathogenesis • After ingestion, S. typhi invade through the gut mucosa to mesenteric lymphoid system then into the bloodstream causing bacteremia. • The incubation period 7 -14 days; (3 -30)days.
Clinical Features • Mild illness (low-grade fever, malaise, dry cough). • Severe (high-grade fever, generalized myalgia, abdominal pain, hepatosplenomegaly, anorexia, . . ). • The classic stepladder rise of fever is relatively rare. In children, diarrhea may be followed by constipation. • Rose spots: - Macular/maculopapular rash. - appear around the 7 -10 th day of the illness. - on the lower chest and abdomen. - last 2 -3 days.
Complications • Hepatitis and cholecystitis. • Intestinal hemorrhage and perforation. • Toxic myocarditis. • Neurologic complications (delirium, psychosis, Guillain-Barre syndrome. . ). • Others: DIC, hemolytic-uremic syndrome, nephrotic syndrome, meningitis and suppurative lymphadenitis.
Differential Diagnosis • Acute gastroenteritis, bronchitis, and bronchopneumonia. • Malaria and sepsis with other bacterial pathogens. • Tuberculosis, brucellosis, Dengue fever, acute hepatitis, infectious mononucleosis. • Others (malignancies, rheumatological, …)
Diagnosis • The mainstay is by a positive culture. - Blood cultures early. - Stool and urine culture after the 1 st wk. • Leukocyte counts frequently low in relation to fever and toxicity. • Thrombocytopenia: severe illness (may accompany DIC). • Liver function test. • Widal test but many false-positive and false-negative results. • Other diagnostic tests: PCR and monoclonal antibodies. • In the developing world the mainstay of diagnosis is clinical.
Treatment • Supportive: adequate rest, hydration, correct fluid and electrolyte. • Antipyretic therapy. • A soft, easily digestible diet if no abdominal distention or ileus. • Antibiotic therapy (chloramphenicol or amoxicillin quinolones or third-generation cephalosporin)
Prevention • Good sanitation services and central chlorination of water. • Avoid consumption of street foods! • Hand washing. Vaccination: (two vaccines) 1. An oral, live-attenuated preparation of S. Typhi, from 6 years of age. 2. The Vi capsular polysaccharide for ≥ 2 years of age. Intramuscular with a booster every 2 years.
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