Medical Microbiology 4th Year Past Paper PDF

Bact: G+ve rods.2 (spore) Micro 3: 4th Year Gram +ve rods: Aerobic :spore forming  Bacillus anthracis General with unique cap...

Bact: G+ve rods.2 (spore) Micro 3: 4th Year Gram +ve rods: Aerobic :spore forming  Bacillus anthracis General with unique capsule composed of D-glutamic acid. characters In humans occurs when persons come into contact with animals dying of anthrax, or Epidemiology &other products contaminated with the bacterial spores. Occupational disease to farmers, slaughters and wool workers. Transmission: People in endemic areas in contact with infected animals (zoonotic disease). The D-glutamic acid capsule is antiphagocytic. Anthrax toxin is made up of 3 proteins: a) Protective antigen (PA) Virulence b) Edema factor (EF) increases cAMP factors c) Lethal factor (LF) induce apoptosis IMP PA binds to specific cell receptors forming a membrane channel entry of EF and LF. PA+ EF edema toxin PA+ LF lethal toxin (major virulence factor) In Humans, entry of spores through injured skin, ingestion or inhalation. The spores germinate in tissue at site of entry (edema and congestion) spread via lymphatics to the blood stream. Pathogenesis session 5 1 Micro 3: 4th Year Cutaneous Anthrax: Malignant pustule (contact with skin) Develops when the spores infect skin usually on the face, neck or arms (eschar). Pneumonic Anthrax: Wool Sartor’s disease Inhalation of spores from dust or wool hair Spores are used in biological war by spreading in the atmosphere. Spores of 1–2 μm in diameter are inhaled the alveolar spaces, transported by lymphatic to lymph nodes germination occurfollowed by toxin production and hemorrhagic mediastinitis  bloody fluid to accumulate in the chest cavitycausing Disease shortness of breath (fatal) Intestinal anthrax: due to ingestion of contaminated meat: has 2 clinical forms:  initial symptoms are nausea, vomiting and anorexia, and fever. Abdominal As the disease progresses, severe abdominal pain, haematemesis, bloody diarrhoea, followed by septicaemia and death. In oro- include sore throat, dysphagia, cervical lymphadenopathy, oedema oesophageal Septicemic anthrax: Complication of the previous forms: 1, 2, 3 Specimen from infected site (skin, sputum, stool) - Chest X-ray Diagnosis Endoscopy to diagnose intestinal anthrax. - PCR and immunofluorescence 1. Parenteral penicillin or tetracycline until the edema settles oral therapy is given for a 5-7 days. Treatment: 2. Ciprofloxacin used for modified strains & in biological war. 3. Incision and drainage should not be performed 1. Infected animals (main source) should be burned or burred in lime Prevention and 2. Sterilization of wool products. control 3. Immunization with Pasteur vaccine (living attenuated Bacillus anthracis by cultivation at 42oC to 43oC). session 5 2 Micro 3: 4th Year Bacillus cereus: Can grow in food and causes food poisoning Produce toxins that cause the disease (intoxication rather than food borne infection) IMP live cells are not required for intoxication. Self-limiting and recovery occur within 24 hours. - Gram positive - Spore forming Properties - Motile - Facultative anaerobe - Spores are resistant to gastric acidity Transmission - foodborne 2 types of toxins: 1. Diarrheal toxin: heat labile enterotoxins 2. Emetic toxin: (Heat stable enterotoxins ) Cyclic peptide – cereulide: resistant to Virulence factors: gastric acid, proteolysis and heat. N.B: Can cause ocular infections (necrotic toxin, phosopholipase) Diarrheal syndrome: ‘Long- incubation’ form The food along with B. cereus is consumed, the site of toxin production is small intestine. Disease Emetic syndrome - following ingestion of food with preformed toxin  The Diarrheal form is diagnosed by isolation of the organism from stool and food. (Meat and Vegetables) Diagnosis  The Emetic form is diagnosed by isolating the organism from the incriminated food (Rice and Pasta) Treatment - Self-limiting and recovery occur within 24 hours. session 5 3 Micro 3: 4th Year Gram +ve rods: Spore forming: Anaerobic pathogenic Clostridium species  C. tetani  C. perfringens  C. botulinum  C. difficile Clostridium tetani: causing tetanus - Motile rod with terminal bulging spores (Drum-stick appearance) - Clostridium tetani is highly resistant. - It is a spore-forming General - can withstand extreme temperature conditions. characteristics: - Tetanus development depends: the immunization status of the individual local conditions in the wound. Mode of Spores introduced into wounds by contaminated soil or foreign objects such as nail transmission in deep wounds? IMP In aerobic surfacebacteria die * Low O2 environment bacteria thrive - In developing countries children secondary to wounds. Epidemiology - in neonates with contaminated umbilical stump after labor or abortion - surgical procedures performed with nonsterile instruments. Virulence - potent tetanospasmin neurotoxin. factors: - It enters the CNS at the neural junctions  travels along the spinal cord. - It prevents the inhibitory neurotransmitter release in synapses  muscle tone, Pathogenesis muscular rigidity and spasm - No invasiveness session 5 4 Micro 3: 4th Year Trismus or “lockjaw”: An early sign due to an  in muscle tone and spasm in the masseter muscle. “Risus Sardonicus”. Disease Muscular rigidity and reflex spasms painful opisthotonos, abdominal rigidity Opisthotonos (a spasmhead, heels bent backward) precipitated by stimuli such as touch or changes in the level of noise or light. Spasm of respiratory muscles  ventilation and hypoxemia. - Depends on the characteristic clinical signs of muscle spasm - lesser extent upon the history - In 2/3 of cases C. tetani could not be isolated from cultures of the wound Diagnosis - C. tetani can be recovered from the wound in only about one-third of the cases, so laboratory tests are not helpful for diagnosis. Specimen from wound exudates. - Microscopic examination: (Drum-stick appearance). treatment of tetanus requires important factors: 1- cleaning of the wound & surgical removal of affected tissues Treatment: 2- Stimulation of the patient should be kept to a minimum. IMP 3- Passive immunization: Tetanus-immune globulin (TIG) should be administered (I.M) at a dosage of 500 units immediately. 4- Diazepam is extremely effective in inducing muscle relaxation and sedation. 1- Active immunization with injections of combined vaccine (DPT): diphtheria + pertussis+ tetanus toxoid in children. Prevention: - A booster injection every 10 years is recommended 2- Pregnant ladies in the third trimester could receive tetanus toxoid in order to provide their neonates transplacentally specific antibodies. session 5 5 Micro 3: 4th Year Clostridium botulinum: causing food poisoning caused by 8 distinct polypeptides toxins (A-H) produced by the C. botulinumthe most potent toxins known. Types A, B and E are the most common causes of botulism in man. Pathogenesis associated with ingestion of sausage, canned foods. Type “E” botulism is usually associated with fish products. These toxins interfere with neurotransmission at peripheral cholinergic synapses preventing the release of acetylcholine. Occurs in 3 forms: 1. Food poisoning: eating food that contains the toxin. Disease 2. Wound botulism: toxin is produced by organisms contaminating a wound. 3. Infant botulism: toxin production by organisms within the GIT of infants (Floppy baby syndrome) Symmetrical, descending flaccid paralysis that begins within hours to a few days Postural hypotension - Dilated pupils due to ocular paralysis - Dry mucous membranes, clinical Pharyngeal paralysis resulting in aphonia manifestation Absence of fever or GIT symptoms. Death is due to respiratory paralysis. The diagnosis must be suspected on clinical signs Lab The botulinum toxin could be demonstrated in the patient's serum or stool by injecting Diagnosis serum or stool extract into mice and looking for signs of botulism. Treatment: Polyvalent antibody: as once the toxin bounds to nervous cells never dissociate easily. Prevention Sterilization of canned food session 5 6 Micro 3: 4th Year Clostridium perfringens: Causing gas gangrene More open superficial wounds less likely to become infected especially if properly Transmission cleaned and dressed compared to deeper penetrating wounds Only 5% of wounds colonized with clostridial organisms develop an infection. A deep penetrating wound into muscle tissue in which Epidemiology the host is immunocompromised is more likely to develop infection compared to a host with a healthy immune system. Clostridium perfringens produces 17 known toxins: (necrotizing activity of gas gangrene). α-toxin ❖ Lecithinase (or phospholipase) that breaks down cell (alpha): membrane cell death and tissue necrosis. β-toxin ❖ has necrotic (tissue death) activity. Virulence (beta): factors δ-toxin ❖ has blood destructing and breakdown of leukocytes. IMP (theta): Collagenase ❖ breaks down connective tissue allowing the rapid spread of (k-toxin) the organism Enterotoxin ❖ Causes intestinal damagealter membrane permeability - Gas gangrene involving muscle extremeties where anaerobiasis can occur. Enzymes: Hyaluronidase – Proteinase – Collagenase Gas gangrene (myonecrosis) is a highly lethal infection - Characterized by rapidly progressive gangrene of the injured tissue along with the production of foul-smelling gas. - Life threatening infection of skeletal muscle). - The earliest symptoms of gas gangrene are intense pain, low-grade fever, edema, and a sweet-odorous discharge (6 h to 3 days). Disease - Within few hours, the entire region may become edematous. - Gas produced by clostridia may produce a crackling sensation when the affected area is pressed - Progressing to a bronze, brown, or black color. - Foul-smelling brown-red or bloody discharge drips from the affected tissues or wound. - Septic shock which is life threatening session 5 7 Micro 3: 4th Year Histological specimen or wound exudates. Lab Gram stain: Gram-positive capsulated rods, non-motile. Diagnosis Nagler's reaction detects the Lecithinase Lecithinase (α-toxin; phospholipase) hydrolyzes phospholipids in egg-yolk agar Without treatment death occurs in 2 days. Prompt surgical removal of dead, damaged, and infected tissue is necessary. Treatment: Antibioticsshould be given in big doses. Analgesics may be required to control pain. Hyperbaric oxygen and chelating agents on affected limb can help. NB: C. perfringens in presence of other four species of clostridia cause the disease gas gangrene 4-Clostridium difficile Prosperities: This organism is present in the GIT. If normal flora of intestine is altered by antibiotic therapy Epidemiology C.difficile can grow and colonize Virulence produces an enterotoxin causing fluid accumulation in the intestine. factors: (Pseudomembranous colitis) (PC): Disease ❖ include abdominal pain with a watery diarrhea and leukocytosis "Pseudomembranes" consisting of fibrin, mucus and leukocytes Diagnosis Pseudomembranes observed by colonoscopy. Treatment: Discontinuation of initial antibiotic (e.g. ampicillin) Specific antibiotic therapy (e.g. vancomycin) session 5 8