BackNervous and Digestive System Infections: Microbiology Study Notes
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Other Nervous System Infections
Fungal Infections of the Central Nervous System
Fungal infections of the CNS are rare but can be severe, especially in immunocompromised individuals. Only a few fungi are primary pathogens capable of causing disease in healthy hosts.
Fungal spores are ubiquitous in the environment (dirt, air, water).
Prevention of all fungal diseases is nearly impossible due to widespread spores.
Immunocompromised patients are at higher risk for CNS fungal infections.
Cryptococcosis
Cryptococcosis is a fungal infection primarily affecting immunocompromised individuals, notably those with HIV/AIDS.
Etiological agent: Cryptococcus neoformans (yeast-like fungus)
Forms tough, resistant spores
Transmission: Inhalation of aerosolized bird droppings (e.g., pigeons)
Mechanism: Fungus enters lungs, invades macrophages, migrates to lymphatic system, can infect blood and invade CNS
Causative agent | Cryptococcus neoformans and C. gattii fungi |
|---|---|
Epidemiology | Over 1 million cases annually, mostly in immunocompromised patients; high mortality in sub-Saharan Africa |
Transmission | Inhalation of spores from bird droppings |
Signs & symptoms | Cough, flu-like symptoms, fever, headache, agitation, seizures |
Diagnosis | Cultures, microscopic methods, antigen detection in CSF |
Protozoan Nervous System Infections
Protozoans are single-celled eukaryotic parasites with complex life cycles. Some flagellated and amoeboid protozoans cause serious neurological symptoms in humans.
Facultative anaerobes
Reproduce sexually or asexually depending on life stage
African Sleeping Sickness
African sleeping sickness is a tropical disease found in Africa, caused by Trypanosoma brucei.
Subspecies: T. brucei rhodesiense (acute, often fatal), T. brucei gambiense (chronic, 98% of cases)
Transmission: Tsetse fly bite
Symptoms: Chancre at bite site, fever, headache, swollen lymph nodes, sleep disturbances
Progression: Parasite enters blood, crosses blood-brain barrier, infects CNS
Mechanism: Direct cytotoxic effects, strong immune reaction can damage host neurons
Complications: Fatal if untreated
Primary Amoebic Meningoencephalitis (PAM)
PAM is a rare but almost always fatal CNS infection caused by Naegleria fowleri, a thermophilic amoeba.
Transmission: Swimming in warm, stagnant water; use of nonboiled tap water in neti pots
Mechanism: Amoeba enters nasal passages, burrows into mucosa, travels up olfactory nerves to brain
Symptoms: Intense headache, sore throat, vomiting, fever, stiff neck, seizures, hallucinations, coma
Progression: Death usually occurs within 1-2 weeks
Complications: Postmortem shows hundreds of trophozoites in brain; CSF filled with protozoans and dead WBCs
Other agents: Acanthamoeba spp., Balamuthia mandrillaris (similar transmission and symptoms, reside in host for 3-24 months before symptoms, almost always fatal)
Toxoplasmosis
Toxoplasmosis is a protozoan infection caused by Toxoplasma gondii, with cats as the definitive host.
Transmission: Cat feces, contaminated water, undercooked meat, congenital
Mechanism: Oocysts consumed, develop into tachyzoites, invade tissues; can cross placenta in pregnant women
Prevention: Immunocompromised and pregnant women should avoid litter boxes
Symptoms: Usually asymptomatic; in immunocompromised, cysts rupture causing encephalitis (confusion, headache, fever); in pregnancy, miscarriage or stillbirth
Progression: Untreated cases may result in seizures, psychiatric symptoms, coma, death
Causative agent | Toxoplasma gondii, a protozoan |
|---|---|
Epidemiology | Up to 23% of US population exposed; mostly asymptomatic; severe disease in immunocompromised and pregnancy |
Transmission | Undercooked meat, cat feces, congenital |
Signs & symptoms | Asymptomatic or flu-like; severe cases: encephalitis, miscarriage |
Diagnosis | Serology, PCR, ELISA |
Transmissible Spongiform Encephalopathy (TSE)
TSEs are fatal neurodegenerative diseases caused by prions (infectious proteins).
Etiological agent: Prions
Transmission: vCJD from BSE-contaminated beef; Creutzfeldt-Jakob disease is spontaneous
Symptoms: Memory loss, difficulty speaking, tremors, death
Progression: Brain tissue develops sponge-like appearance
Mechanism: PrPC encounters abnormal PrPSC, becomes infectious, transforms more PrPC, prions clump and kill neurons, dead cell pockets cause sponge-like brain tissue
Causative agent | Prions |
|---|---|
Epidemiology | Median age of death for CJD is 68 years; vCJD median age is 28 years; rare in US |
Transmission | vCJD: contaminated beef; CJD: spontaneous, genetic, or iatrogenic |
Signs & symptoms | Rapid dementia, memory loss, speech impairment, ataxia |
Diagnosis | Clinical history, EEG, MRI, brain biopsy |
Digestive System Infections
Digestive System Anatomy and Defenses
The digestive system includes the gastrointestinal (GI) tract and accessory organs, and is a major entry portal for pathogens.
GI tract: Mouth to anus; upper GI (mouth, pharynx, esophagus, stomach), lower GI (small/large intestines, rectum, anus)
Accessory organs: Salivary glands, liver, gallbladder, pancreas
Lymphatic tissues: Tonsils, appendix, Peyer's patches
Upper GI Tract
Food enters at mouth; salivary glands secrete enzymes for lipid/carbohydrate digestion
Stomach mixes food with gastric juices, begins protein digestion, acidic environment limits microbial growth
Food and gastric juices form chyme
Lower GI Tract
Chyme enters small intestine; bile (from liver, stored in gallbladder) aids fat digestion
Bile salts inhibit growth of many bacteria, especially Gram-positive
Pancreas secretes digestive substances
Liver stores nutrients, metabolizes drugs/toxins, receives nutrient-rich blood from small intestine
Large intestine absorbs water and water-soluble vitamins; undigested matter excreted as feces
Digestive System Defenses
Lysozyme in saliva
Acidity of gastric juices
Mucosa-associated lymphoid tissue (MALT)
Specific immune cells and lymphatic tissue
Digestive System Microbiome
The digestive tract hosts the most diverse microbiome in the body, with thousands of species.
Mouth: Streptococcus species most common; teeth colonized by Streptococcus, Neisseria, Fusobacterium, Actinomyces
Feces: Rich in Bacteroides species; fungi (e.g., Candida) and some protozoa present but bacteria predominate
Roles: Compete for nutrients, excrete antimicrobials, assist digestion, produce nutrients (e.g., Escherichia coli produces vitamin K), impact metabolism, obesity, immune responses
Gastrointestinal Infection Symptoms and Diagnostic Tools
GI infections can cause a range of symptoms and are diagnosed using various clinical and laboratory methods.
Diarrhea: Frequent passing of loose or watery stool
Enteritis: Inflammation of intestines
Gastritis: Inflammation of stomach
Gastroenteritis: Inflammation of stomach and intestines
Dysentery: Diarrhea with pain, blood, and/or mucus
Dehydration: Excessive loss of body fluid
Hypovolemic shock: Low blood volume, can lead to organ failure
Transmission and Epidemiology
Most GI pathogens transmit via the fecal-oral route (contaminated food/water)
Hand washing, sanitation, and food safety regulations reduce transmission
CDC estimates 1 in 6 Americans suffer foodborne illness yearly; higher prevalence in developing nations
Diarrhea and dysentery kill about 2.2 million people annually, mostly children under five in developing countries
Diagnostic Tools
Fecal sample collection and culture on selective/differential media (e.g., MacConkey agar)
Molecular diagnostics and microscopic examination for parasites/eggs
Endoscopy (upper GI: via mouth; lower GI: colonoscopy via anus) to observe tissue damage