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Tetanus: Etiological agent
Clostridium tetani (endospore)
Tetanus: Taxonomic classification
Gram positive bacterium (bacilli)
Tetanus: Transmission
parenteral route introduces spores
- Spores of C. tetani enter the body through a puncture wound
- Spores encyst in a scab creating an anaerobic environment
- C. tetani proliferate, producing the neurotoxin tetanospasmin
- Accumulation of the toxin causes spasming of the muscles
Tetanus: Significant symptoms
Accumulation of the toxin causes spasming of the muscles
- Typically, first muscles to experience spasming are the jaws (lockjaw) and
face (rictus grin)
- Spasming (tetany) of the chest, neck, back, and buttocks can result in
opisthotonos (arching of the whole body), fractures and muscle tearing
Tetanus: Diagnosis, treatment, and prevention
Diagnosis: recognition of symptoms
Treatment: monoclonal antibody therapy, antibiotics (metronidazole, benzodiazepines to control muscle spasms, tracheotomy and ventilation
Prevention: DPR vaccine, prophylaxis boosters, wound care, avoiding
risky behaviors
Tetanus: Other
Prevalence: >209,000 cases worldwide annually
Mortality: ~10% (respiratory and muscular paralysis)
Botulism: Etiological agent
Clostridium botulinum (durable endospores)
Botulism: Taxonomic classification
Gram positive bacterium (bacilli)
Botulism: Transmission
Primarily through consumption of tainted food (Likely anaerobically sealed food packaged w/o O2 like a can or jar)
- C. botulinum grows in anaerobic environments, and produces one of many types of neurotoxins
- Consumption of food tainted with the neurotoxin begins intoxication
Botulism: Significant symptoms
- Initial symptoms are similar to other forms of food poisoning;
nausea, abdominal and lack of fever
- As accumulation of neurotoxin progresses, blurred vision, progressive flaccid paralysis, reduced muscle movement, and dyspnea (labored breathing)
- Untreated symptoms can lead to total paralysis
Botulism: Diagnosis, treatment, and prevention
Diagnosis: identification of symptoms, testing for spores and/or neurotoxin in stool
Treatment: antitoxin
Prevention: avoiding spoiled food
Botulism: Other
Mortality: 7.5% (respiratory and muscular paralysis)
Prevalence: >1,000 cases worldwide annually
Listeriosis: Etiological agent
Listeria monocytogenes
Listeriosis: Taxonomic classification
Gram positive bacterium (bacilli)
Listeriosis: Transmission
- consumption of tainted food (usually cold foods, high in sugar, high fat), vertical transmission from mother to fetus
- Consumption of tainted foods with L. monocytogenes allows the bacterium to enter the body
Listeriosis: Significant symptoms
- The bacterium produces beta hemolysin in the bloodstream, causing systemic symptoms such as fever, muscle aches, and diarrhea
- Accumulation of the bacterium in the nervous system causes meningitis (swelling of the meninges) and encephalitis (swelling of the brain)
- Prolonged infection can lead to sepsis
Listeriosis: Diagnosis, treatment, and prevention
Diagnosis: isolation of bacterium from blood or CSF
Treatment: antibiotics (ampicillin)
Prevention: hygiene and sanitation, avoiding soft cheese in "at-risk"
group
Listeriosis: Other
- Prevalence: >1,600 cases worldwide annually
Mortality: ~16% (sepsis, meningitis, encephalitits)
- Fetal mortality: ~ 22%
- Leading cause of foodborne death in the US
Lyme disease: Etiological agent
Borrelia sp.
Lyme Disease: Taxonomic classification
Gram negative bacterium (spirochetes)
Lyme Disease: Transmission
bite of an infected Ixodes sp. ticks (KNOW TICK)
- An infected tick or flea bites a patient, introducing the bacteria
- Spirochetes colonize the bloodstream and lymphatic system
Lyme Disease: Significant symptoms
- At the site of infection, waves of inflammation causes bull's eye rash
- Systemic symptoms include fatigue, headache, body aches, fever,
chills, muscle pain, joint pain
- Neurological symptoms include aseptic meningitis, photosensitivity, partial loss of vision, facial palsy, impaired motor or sensory functions, arthritis
Lyme Disease: Diagnosis, treatment, and prevention
Diagnosis: recognition of symptoms (Bullseye rash), serological testing
Treatment: antibiotics (doxycycline)
Prevention: insect repellent, avoiding risk areas, pet control, wearing long sleeves/legged clothes (Keeping ticks off body)
Lyme Disease: Other
Prevalence: 25,000 cases worldwide annually
Seasonal: (April - September)
Mortality:
Hansen's Disease (Leprosy): Etiological agent
Mycobacterium leprae
Hansen's Disease (Leprosy): Taxonomic classification
Acid-fast bacterium (bacilli)
Hansen's Disease (Leprosy): Transmission
direct contact with infected persons or animal vectors
- Mechanism for transmission for M. leprae is mostly unknown
- Once the bacterium is in the body, it disseminates through the nervous
system, causing systemic infection
Leprosy: Significant symptoms
Systemic symptoms include runny nose, and muscle weakness
- Neurological symptoms include loss of sensation in the extremities
- Skin symptoms include dry skin, discoloration of the skin, thickening of the facial skin
Leprosy: Diagnosis, treatment, and prevention
Diagnosis: recognition of symptoms, neurological testing (poke with needle and ask if it hurt), acid-fast staining
Treatment: multi-drug therapy
Prevention: avoiding contact with infected persons, avoiding armadillos
Leprosy: Other
Prevalence: >200,000 cases worldwide annually
Mortality: ~2% (organ failure) facial lesions
Cryptococcosis: Etiological agent
Cryptococcus sp.
Cryptococcosis: Taxonomic classification
Fungus (yeast)
Cryptococcosis: Transmission
inhalation of fungal spores
Inhalation of Cryptococcal spore will allow the spores to germinate in the lungs and become yeast like
- Initial germination causes reparatory symptoms
Cryptococcosis: Significant symptoms
Initial germination causes reparatory symptoms such as cough, shortness of breath, chest pain and fever
- As a yeast, they will disseminate into central nervous system, encapsulating on the brain and meninges
- At the yeast grows, waste produces will cause headache, fever, neck pain, nausea, vomiting, photosensitivity, confusion, and meningitis
Cryptococcosis: Diagnosis, treatment, and prevention
- Diagnosis: agglutination of antigens in serum or CSF
- Treatment: antifungals (amphotericin B)
- Prevention: avoiding bird droppings, regular screening in "at-risk" groups, prophylactic antifungals
Cryptococcosis: Other
- Prevalence: >900 cases worldwide annually
- Mortality: 60% (meningitis, complications in the brain)
Poliomyelitis: Etiological agent
Poliovirus
Poliomyelitis: Taxonomic classification
Group IV nonenveloped icosahedral virus
Poliomyelitis: Transmission
consumption of tainted water
- The host ingests water tainted with poliovirus
-Poliovirus enters the GI system by binding to CD155n receptor of the endothelium
-The virus replicates in the GI system, causing GI symptoms such as sore throat, low fever and abdominal discomfort
Poliomyelitis: Significant symptoms
- The virus replicates in the GI system, causing GI symptoms such as sore throat, low fever and abdominal discomfort
- If the virus disseminates to the central nervous system, the infection becomes more severe
- Neurological symptoms include headache, neck pain, back pain, abdominal pain, extremity pain, fever, vomiting, lethargy, aseptic meningitis, and paralysis
Poliomyelitis: Diagnosis, treatment, and prevention
Diagnosis: identification of flaccid paralysis, identification of virus in stool sample
Treatment: analgesics for pain, physical therapy, surgery, respirators
Prevention: hygiene and sanitation, polio vaccine
Poliomyelitis: Other
Prevalence: >600 cases worldwide annually
Mortality: 2 - 75% (respiratory and muscular paralysis, meningitis)
Rabies: Etiological agent
Rabies lyssavirus
Rabies: Taxonomic classification
Group V nonenveloped helical virus
Rabies: Transmission
being bitten by an afflicted animal
The host is bitten by an animal infect with rabies, and the virus is transmitted through the saliva
The virus will slowly divide in the host's nervous system for months
Rabies: Significant symptoms
- First symptoms are typical general and systemic, such as fever or headache
- As symptoms progress, the patient can display aggressive neurological symptoms, such as meningitis, paralysis, anxiety, insomnia, confusion, agitation, abnormal psychological behaviors, photosensitivity, paranoia, terror, hallucinations, delirium, and coma
- Some patients will develop "dumb" rabies, with less aggressive symptoms like lethargy,
depression, loss of coordination, and coma
Rabies: Diagnosis, treatment, and prevention
Diagnosis: identification bite through patient history
Treatment: rabies vaccine "after-bite"
Prevention: rabies vaccines, vaccinating animals, pet control, avoiding wild animals
Rabies: Other
Prevalence: Endemic
Mortality: Nearly ALWAYS Fatal (cardio-respiratory arrest, paralysis)
Trypanosomiasis: Etiological agent
Trypanosoma brucei

Trypanosomiasis: Taxonomic classification
Flagellated protozoan (Mastigophora)
Lifestyle: obligate parasite (human = intermediate host)
Trypanosomiasis: Transmission
being bitten a Tsetse fly
- The host is bitten by Tsetse fly, and the fly deposits the trophozoites in saliva
- The trophozoites travel through the blood vessels to the central nervous system
- Matured trophozoites cause systemic symptoms through production of waste products
Trypanosomiasis: Significant symptoms
- Matured trophozoites cause systemic symptoms through production of waste products such as fever, headache, joint pain, itching, weakness, fatigue, enlargement of the liver and spleen, swelling of the lymph nodes
- As the infection progresses, severe symptoms develop, such as sleep-wake inversion, tremors, hemiparesis, hallucinations, anxiety, delirium, mania, confusion, coma
Trypanosomiasis: Diagnosis, treatment, and prevention
Diagnosis: microscopy of ulcer fluid, blood or CSF for parasitemia
Treatment: antiprotozoals (fexinidazole)
Prevention: insect repellent, avoiding risk areas, wearing long sleeved/legged clothing, fly traps
Trypanosomiasis: Other
Prevalence: <600 cases worldwide annually
Mortality: FATAL if untreated (coma, organ failure)
Variant Creutzfeldt-Jakob Disease (Mad
Cow: Etiological agent
PrPSc
VCJD (Mad
Cow): Taxonomic classification
prion
Mad Cow Disease: Transmission
Consumption of tainted meats, or contact with tainted blood or semen
The prion is consumed in tainted meat
Through methods unknown, the prion converts healthy proteins in the brain into infectious prions
- As prions accumulate in the brain, the brain tissue will begin to congregate together in spongiform encephalopathy
-Neurological symptoms begin to manifest shortly after

Mad Cow Disease: Significant symptoms
Patients will display psychiatric problems, behavioral changes, extreme pain, loss of coordination, dementia, involuntary muscle movements
Mad Cow Disease: Other
Prevalence:
Kuru
(isolated case of prionic diseases) Kuru is caused by a prion from the same family as VCJD
- The prion is consumed in tainted meat
- Through methods unknown, the prion converts healthy proteins in the brain into infectious prions
- As prions accumulate in the brain, the brain tissue will begin to congregate together in spongiform encephalopathy
- Neurological symptoms begin to manifest shortly after
- Patients will display headache, joint pain, unsteady gait, decrease muscle control, dysarthria (inability to speak), tremors, uncontrollable sporadic laughter, dysphagia (inability to swallow)
Mortality: ALWAYS FATAL (destruction of the brain and spinal cord)
Mad Cow Disease nd kuru: Diagnosis, treatment, and prevention
- Diagnosis: examination of brain tissue
- Treatment: none.
- Prevention: avoiding tainted beef products, avoiding tainted blood/blood transfusions, condoms
- For Kuru, avoiding cannibalism