By Z. Zapotek. Northwestern College, Iowa.

Most cases recover discount 20 mg levitra fast delivery, if diagnosed and treated promptly order levitra 20 mg on line, including early administration of antitoxin and intensive respiratory care order 10 mg levitra free shipping. Ingested spores germinate and produce bacteria that reproduce in the gut and release toxin. In most adults and children over 6 months, germination would not happen because natural defences prevent germination and growth of Clostridium botulinum. Clinical symptoms in infants include constipa- tion, loss of appetite, weakness, an altered cry, and a striking loss of head control. Infant botulism has in some cases been associated with ingestion of honey contaminated with botulism spores, and mothers are warned not to feed raw honey to their infants. The case fatality rate of hospitalized cases is less than 1%; it is much higher without access to hospitals with paediatric intensive care units. Diagnosis of foodborne botulism is made by demonstration of botuli- num toxin in serum, stool, gastric aspirate or incriminated food; or through culture of C. Identification of organisms in suspected food is helpful but not diagnostic because botulinum spores are ubiquitous; the presence of toxin in suspect food source is more significant. The diagnosis may be accepted in a person with the clinical syndrome who had consumed a food item incriminated in a laboratory-confirmed case. Electromyogra- phy with rapid repetitive stimulation can corroborate the clinical diagnosis for all forms of botulism. Infectious agent—Foodborne botulism is caused by toxins pro- duced by Clostridium botulinum, a spore-forming obligate anaerobic bacillus. Most human outbreaks are due to types A, B, E and rarely F; type G has been isolated from soil and autopsy specimens but a causal role in botulism is not established. Type E outbreaks are usually related to Clostridium botulinum fish, seafood and meat from marine mammals. Proteolytic (A, some B and F) and nonproteolytic (E, some B and F) groups differ in water activity, temperature, pH and salt requirements for growth. Toxin is produced in improperly processed, canned, low acid or alkaline foods, and in pasteurized and lightly cured foods held without refrigeration, especially in airtight packaging. Occurrence—Worldwide; sporadic cases, family and general out- breaks occur where food is prepared or preserved by methods that do not destroy spores and permit toxin formation. Cases rarely result from commercially processed products; outbreaks have occurred from contam- ination through cans damaged after processing. Cases of intestinal botu- lism have been reported from the Americas, Asia, Australia and Europe. Actual incidence and distribution of intestinal botulism are unknown because physician awareness and diagnostic testing remain limited. Reservoir—Spores, ubiquitous in soil worldwide; are frequently recovered from agricultural products, including honey, and also found in marine sediments and in the intestinal tract of animals, including fish. Growth of this anaerobic bacteria and formation of toxin tend to occur in products with low oxygen content and the right combination of storage temperature and preservative parameters, as is most often the case in lightly preserved foods such as fermented, salted or smoked fish and meat products and in inadequately processed home-canned or home- bottled low acid foods such as vegetables. Poisonings are often due to home-canned vegetables and fruits; meat is an infrequent vehicle. Several outbreaks have occurred following con- sumption of uneviscerated fish, baked potatoes, improperly handled commercial potpies, saute´ed onions, minced garlic in oil. Garden foods such as tomatoes, formerly considered too acidic to support growth of C. In Canada and Alaska, outbreaks have been associated with seal meat, smoked salmon and fermented salmon eggs. In Europe, most cases are due to sausages and smoked or preserved meats; in Japan, to seafood. Inhalation botulism, following inhalation of the toxin (aerosol), has occurred in laboratory workers. In these cases, neurological symptoms may be the same as in foodborne botulism, but the incubation period may be longer. Waterborne botulism could theoretically also result from the ingestion of the preformed toxin. Wound botulism often results from contamination of wounds by ground-in soil or gravel or from improperly treated open fractures. It has been reported among chronic drug abusers (primarily in dermal abscesses from subcutaneous injection of heroin and also from sinusitis in cocaine “sniffers”). Intestinal botulism arises from ingestion of spores that germinate in the colon, rather than through ingestion of preformed toxin. Incubation period—Neurological symptoms of foodborne botu- lism usually appear within 12–36 hours, sometimes several days after eating contaminated food. The shorter the incubation period, the more severe the disease and the higher the case-fatality rate. The incubation period of intestinal botulism in infants is unknown, since the precise time of ingestion often cannot be determined. Almost all patients hospi- talized with intestinal botulism are between 2 weeks and 1 year old; 94% are less than 6 months; the median age at onset was 13 weeks. Preventive measures: Good practices in food preparation (particularly preservation) and hygiene; inactivation of bacterial spores in heat-sterilized, canned products or inhibition of growth in all other products. Commercial heat pasteurization (vacuum-packed pasteurized products, hot smoked products) may not suffice to kill all spores and the safety of these products must be based on preventing growth and toxin production. Refrigeration combined with control of salt content and/or acidity will prevent the growth or formation of toxin. If exposure to the toxin via an aerosol is suspected, the patient’s clothing must be removed and stored in plastic bags until it can be washed with soap and water. Food and water samples associated with suspect cases must be obtained immediately, stored in sealed containers and sent to reference laboratories. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Case report of suspected and confirmed cases obligatory in most countries, Class 2 (see Reporting); immediate telephone report indicated. Sterilize contaminated utensils by boiling or by chlorine disinfection to inactivate any remaining toxin. Those known to have eaten the incriminated food should be purged with cathartics, given gastric lavage and high ene- mas and kept under close medical observation. Serum should be collected to identify the specific toxin before antitoxin is administered, but antitoxin should not be withheld pending test results. Immediate access to an intensive care unit is essential so that respiratory failure, the usual cause of death, can be anticipated and managed promptly. For wound botulism, in addition to antitoxin, the wound should be debrided and/or drainage established, with appropriate antibiotics (e. Equine botulinum antitoxin is not used because of the hazard of sensitization and anaphylaxis. Anti- biotics do not improve the course of the disease, and aminoglycoside antibiotics in particular may worsen it by causing a synergistic neuromuscular blockade. Epidemic measures: Suspicion of a single case of botulism should immediately raise the question of a group outbreak involving a family or others who have shared a common food. Home-preserved foods are the prime suspect until ruled out, although restaurant foods or widely distributed commercially preserved foods are occasionally identified as the source of intoxication and pose a greater public health threat. Recent outbreaks have implicated unusual food items, and even unlikely foods should be considered.

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Susceptibility and resistance—Susceptibility is variable; immu- nity apparently does not follow attack order 20mg levitra with amex. Preventive measures: Except for those measures applicable only to syphilis cheap levitra 20mg free shipping, preventive measures are those for Syphilis cheap 20mg levitra with amex, 9A. Educational programs in endemic areas should stress the impor- tance of early diagnosis and treatment. Control of patient, contacts and the immediate environment: 1) Report to local health authority: A reportable disease in most states and countries, Class 3 (see Reporting). Erythromycin, trimethoprim-sufamethox- azole and doxycycline have been reported to be effective but drug-resistant strains of the organism occur. Treatment is continued for 3 weeks or until the lesions have resolved; recurrence is not rare but usually responds to a repeat course unless malignancy is present. Many of these agents have been isolated from rodents but are not associated with human cases. Because they are caused by related causal organisms and have similar features of epidemiology and pathology (febrile prodrome, thrombocyto- penia, leukocytosis and capillary leakage), both the renal and the pulmo- nary syndrome are presented under Hantaviral diseases. Identification—Acute zoonotic viral disease with abrupt onset of fever, lower back pain, varying degrees of hemorrhagic manifestations and renal involvement. Severe illness is associated with Hantaan (primarily in Asia) and Dobrava viruses (in the Balkans). Disease is characterized by 5 clinical phases which frequently overlap: febrile, hypotensive, oliguric, diuretic and convalescent. High fever, headache, malaise and anorexia, followed by severe abdominal or lower back pain, often accompanied by nausea and vomiting, facial flushing, petechiae and conjunctival injection characterize the febrile phase, which lasts 3–7 days. The hypotensive phase lasts from several hours to 3 days and is characterized by deferves- cence and abrupt onset of hypotension, which may progress to shock and more apparent hemorrhagic manifestations. Blood pressure returns to normal or is high in the oliguric phase (3–7 days); nausea and vomiting may persist, severe hemorrhage may occur and urinary output falls dramatically. The majority of deaths (the case-fatality rate ranges from 5% to 15%) occur during the hypotensive and oliguric phases. Diuresis heralds the onset of recovery in most cases, with polyuria of 3–6 liters per day. A less severe illness (case-fatality rate 1%) caused by Puumala virus and referred to as nephropathia epidemica is predominant in Europe. Infec- tions caused by Seoul virus, carried by brown or Norway rats, are clinically milder, although severe disease may occur with this strain. Hantavi- ruses can be propagated in a limited range of cell cultures and laboratory rats and mice, mainly for research purposes. Leptospirosis and rickettsio- ses must be considered in the differential diagnosis. More than 25 antigenically distinguishable viral species exist, each associ- ated primarily with a single rodent species. Seoul virus is found world- wide, Puumala virus in Europe, Hantaan virus principally in Asia, less often in Europe, Dobrava (Belgrade) virus in Serbia and Montenegro (formerly the Federal Republic of Yugoslavia). In 1951, it was recognized among United Nations troops in Asia and later in both military personnel and civilians—the virus was first isolated from a field rodent (Apodemus agrarius) in 1977 near the Hantaan river. The disease is considered a major public health problem in China and the Republic of Korea. Occurrence is seasonal, most cases occurring in late autumn and early winter, primarily among rural populations. In the Balkans, a severe form of the disease due to Dobrava virus affects a few hundred people annually, with fatality rates at least as high as those in Asia (5%–15%). Nephropathia epidemica, due to Puumala virus, is found in most of Europe, including the Balkans and the Russian Federation West of the Ural mountains. Seasonal occupational and recreational activities probably influence the risk of exposure, as do climate and other ecological factors of rodent population densities. The availability of newer diagnostic techniques has led to increasing recognition of hantaviruses and hantaviral infections. Mode of transmission—Presumed aerosol transmission from ro- dent excreta (aerosol infectivity has been demonstrated experimentally), though this may not explain all human cases or all forms of inter-rodent transmission. Virus occurs in urine, feces and saliva of persistently infected asymptomatic rodents, with maximal virus concentration in the lungs. Susceptibility—Persons without serological evidence of past infec- tion appear to be uniformly susceptible. Preventive measures: 1) Exclude and prevent rodent access to houses and other buildings. Do not sweep or vacuum rat-contaminated areas; use a wet mop or towels moistened with disinfectant. In so far as possible, avoid inhalation of dust by using approved respirators when cleaning previously unoccupied areas. Control of patient, contacts and the immediate environment: 1) Report to local health authority: In endemic countries where reporting is required, Class 3 (see Reporting). Jostling and the effect of lowered atmospheric pressures during airborne evacuation of cases can be delete- rious to patients critically ill with hantavirus. Epidemic measures: Rodent control; surveillance for hantavi- rus infections in wild rodents. Laboratory-associated outbreaks call for evaluation of the associated rodents and, if positive, elimination of the rodents and thorough disinfection. Disaster implications: Natural disasters and wars often result in increased numbers of rodents and rodent contact with humans. In survivors, recovery from acute illness is rapid, but full convalescence may require weeks to months. Restoration of normal lung function generally occurs, but pulmonary function abnormal- ities may persist in some individuals. Renal and hemorrhagic manifesta- tions are usually absent except in some severe cases. Incidence appears to coincide with the geographic distribution and population density of infected carrier rodents and their infection levels. Reservoir—The major reservoir of Sin Nombre virus appears to be the deer mouse, Peromyscus maniculatus. Antibodies have also been found in other Peromyscus species, pack rats, the chipmunk and other rodents. Other hantavirus strains have been associated mainly with other rodent species of the subfamily Sigmodontinae. Mode of transmission—As with hantaviral hemorrhagic fever with renal syndrome, aerosol transmission from rodent excreta is presumed. The natural history of viral infections of host rodents has not been characterized. Indoor exposure in closed, poorly ventilated homes, vehi- cles and outbuildings with visible rodent infestation is especially impor- tant. Incubation period—Incompletely defined but thought to be ap- proximately 2 weeks with a range of a few days to 6 weeks. Period of communicability—Person-to-person spread of hantavi- ruses has been reported during an outbreak in Argentina.

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The outlook for regrowth worsens when large areas are affected order levitra 10mg without prescription, the patient is over 30 years old and also has atopic dermatitis cheap levitra 20mg otc. Pathology and pathogenesis The disorder is positively associated with autoimmune disorders buy levitra 10 mg with mastercard, including vitiligo and thyrotoxicosis, and it has been assumed that an immune attack is launched against components of the hair follicle. When biopsies are taken from an actively extending patch, a dense ‘bee swarm’-like cluster of lymphocytes can be seen around the follicles. Differential diagnosis Patches of baldness due to hair pulling (trichotillomania) are bizarrely shaped, not as well demarcated as alopecia areata, and have no exclamation mark hairs at 272 Disorders of hair the edge. Tinea capitis is marked by broken hairs and by a degree of redness and scaling of the scalp skin. Disorders that inflame the skin and destroy hair follicles can usually be easily differentiated by the scarring they cause. Treatment Patients with a solitary patch or few patches usually do not need treatment. When the patches coalesce to become a problem cosmetically or when there is alopecia totalis, treatment is often demanded by patients, but is not often effective. All of the above have inconvenient side effects and usu- ally work only while they are being given. Allergic sensitization with 1 per cent diphencyprone causes an eczematous response and ‘kicks’ the follicles back to life in about half the patients and is quite often used. Many patients, having experienced the side effects and frustration of the lack of efficacy of the treatments, decide to cut their losses and disguise their disabil- ity with a wig. Sympathy and support are the most useful applications for this depressing disorder. Diffuse hair loss This is predominantly a problem for middle-aged and elderly women. It is not a single entity and the causes include pattern alopecia, virilization, hypothyroidism, systemic illness such as systemic lupus erythematosus, and drug administration (particularly the anticancer drugs and the systemic retinoids). Ageing also results in a lesser dens- ity of hair follicles, which is more obvious in some subjects than in others. Having considered the above possible causes, there are still some patients with obvious diffuse hair loss for whom there is no adequate explanation. Various defi- ciency states (particularly iron) have been incriminated, but in the majority of instances the supposed deficiency appears to have no other sequel and attempts at its rectification fail to improve the clinical state. If there is no obvious cause for diffuse hair loss, the only medical treatment available is topical minoxidil, but this is unlikely to give substantial benefit. The stimulus causes all the scalp hair follicles to revert to the telogen, or resting, phase. There is a sudden and significant loss of terminal scalp hair some 3 months after the precipitating event, which continues for a few weeks but then spontaneously stops. Traction alopecia Repeated tugging and pulling on the hair shaft may produce loss of hair in the affected areas, such as occurs when hair rollers are used (Fig. It can also develop in young children when they continually rub their scalp on their pillow. Youngsters sometimes tug at their hair, producing the same effect in a bizarre distribution over the scalp (trichitillomania, Fig. Mechanical trauma, burns, bacterial infections and severe inflammatory ringworm of the scalp can produce sufficient damage to cause scarring and permanent hair loss. In discoid lupus erythematosus (see page 79) and lichen planus (see page 144), the scalp skin may be characteristically affected by the dermatosis concerned, but it may be difficult to distinguish these two conditions, even after biopsy. Usually, the affected area is scarred and there is loss of follicular orifices – the few remain- ing being distorted and dilated and containing tufts of hair (Fig. An odd and unexplained type of scalp scarring known as pseudopelade is characterized by small, rounded patches of scarring alopecia without any inflammation. Hair shaft disorders Hair shaft abnormalities may be either congenital or acquired. All long hairs tend to become ‘weathered’ at their ends due to climatic exposure and the usual washing and combing routines. Twisting hairs between the fingers, and other obsessive manipulation of hair, results in a specific type of damage to the hair shafts known as trichorrhexis nodosa, in which expansions of the shaft (nodes) can be seen by routine light microscopy and scanning electron microscopy. Isolated congenital hair shaft disorders include the condition of monilethrix, in which there are spindle-like expansions of the hair shaft at regular intervals (Fig. When the hair growth is on the chin and upper lip, it causes considerable cosmetic embarrassment, even though in most cases it is normal. Disorders of the nails Psoriasis, lichen planus and eczema may all affect the nails, causing characteristic clinical appearances. It also causes well-defined pink/brown areas and onycholysis (separation of the nail plate from the nail bed: Fig. The toenails rarely show these changes, but the nail plates may be thickened, with a yellowish brown discoloration and subungual debris often making it difficult to distinguish from ringworm of the nails. Eczema affecting the fingers may cause irregular deformities of the finger- deformity of the nail plate. In the common form of chronic paronychia, the paronychial skin is thickened and red- dened. It is often tender, and pus may be expressed from the space between the nail fold and the nail plate. The eponychium disappears and the nail plate is often discoloured and deformed (Fig. There is a deep recess between the nail fold and the nail plate, containing debris and micro-organisms, which it is difficult to keep dry. The condition mostly occurs in women whose occupation involves frequent hand washing or other ‘wet’ activities (e. Candida micro-organisms may contribute to the recurrent inflammation to which the affected fingers are subject, but they are not the cause of the disorder. The cause is compounded from mechanical trauma and over-hydration resulting in microbial overgrowth in the nooks and crannies of the nail fold. Treatment The major goals in management are keeping the fingers completely dry and the avoidance of manual work. Providing the advice is taken and the treatment used, patients usually grad- ually improve. It is observed in psoriasis, eczema, chronic paronychia, the ‘yellow nail syndrome’ (see below), thyrotoxicosis, as a result of repeated mechan- ical trauma and for no known reason. The dermatologist told her that this was called onycholysis and was due to her psoriasis. Probably the single most important factor causing this problem is repeated hydration and drying, as in housework, as well as mechanical and chemical trauma. In hypoalbu- minaemia (as in severe liver disease), the lunulae may be lost and the nail plate turns a milky white.

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