Wild Cat II Sch - History

Wild Cat II

(Sch: t. 30)

The second Wild Cat—a wooden-hulled schooner captured by the Federal Navy in 1862—served as a tender to warships of the South Atlantic Blockading Squadron. The vessel was never labeled, and records of her construction and capture have not been found. Her activities and actual duties during that tour are not described in any detail in the available records, but it is known that she operated from St. Helena to Port Royal, S.C.

During that service, she assisted refugees from a plantation attacked by Confederate marauders. On 13 June, Wild Cat sailed up to Hutchinson's Island, off St. Helena Sound, in company with the gig from the sloop-of-war Dale, Lt. W. T. Truxtun, commanding, to investigate a large fire ashore. Upon arrival in the vicinity. the Union sailors found the burning Marsh Plantation, set afire by a marauding Confederate band. The Southern troops had plundered the belongings of the poor negroes there, wounding some, generally striking terror into the hearts of the inhabitants. As Wild Cat sailed up the river, she came in contact with many canoes paddled by panic-stricken former inhabitants of the plantation. Lt. Truxtun soon placed all of the refugees on board Wild Cat and had them transported out of the area. A few days later, while reconnoitering the vicinity, Wild Cat shelled some Confederate raiders spotted near the Ashepoo River.

Wild Cat continued to operate in South Carolina's coastal waters through March of 1865. After a brief spell as pilot boat at Charleston, S.C., in April, the schooner was transferred to the Army on 15 April 1865. Apparently returned to the Navy within three months time, Wild Cat was sold at Charleston on 28 July 1865. Her subsequent fate is unknown.

1975 Northern Michigan Wildcats football team

The 1975 Northern Michigan Wildcats football team represented Northern Michigan University during the 1975 NCAA Division II football season. Led by second-year head coach Gil Krueger, the Wildcats compiled a 13–1 record, with victories over Central Michigan (17–16), Nebraska–Omaha (41–14), Youngstown State (15–0), Eastern Michigan (20–7), and Boise State (24–21) in Idaho in the quarterfinals of the Division II playoffs. [1] [2]

The Wildcats defeated the Western Kentucky in the championship game, 16–14, to win their first Division II national title. [3] [4] [5] [6] [7] The championship game was held at Hughes Stadium in Sacramento, California. Of all current members of Division II, as of 2013, Northern Michigan was the first to win the playoff national championship.

The 1975 team was led by sophomore quarterback Steve Mariucci, [1] later a head coach in the NFL for nine seasons. The previous season in 1974, the Wildcats were winless at 0–10. [3]

Special Events:

Friday, May 28 & Saturday, May 29

Salute to WWII Veterans Ceremony

Location: MCI Center, Washington, DC
May 28: 2:00pm - 4:00pm
May 29: 7:00pm - 9:00pm

* Please note - these events require tickets and are currently sold out. For more information, please see

Saturday, May 29

Memorial Service

Location: Washington National Cathedral, Washington, DC
Time: 10:00am - 11:30am

WWII Memorial Dedication Ceremony

Location: National Mall, Washington DC
Times: 11:00am - Gates Open
12:00pm - 2:00pm -- Pre-show Events (military band performances, video presentations)
2:00pm - 3:30pm -- Ceremony

AP Poll Summary Table
School Pre 11/23 11/30 12/7 12/14 12/21 12/28 1/4 1/11 1/18 1/25 2/1 2/8 2/15 2/22 3/1 3/8 Final

Schedules prior to the 1994-95 season may be missing games vs. non-Division I opponents.

Grumman F4F Wildcat: U.S. Navy Fighter in World War II

Grumman F4F-3 Wildcats of VF-5 (Fighting Squadron 5) fly a tight formation near their home, the aircraft carrier USS Yorktown (CV-5).

‘It was not as you remember it, Saburo. I don’t know how many Wildcats there were, but they seemed to come out of the sun in an endless stream. We never had a chance….Every time we went out we lost more and more planes. Guadalcanal was completely under the enemy’s control….Of all the men who returned with me, only Captain Aito, [Lt. Cmdr. Tadashi] Nakajima and less than six of the other pilots who were in our original group of 80 men survived.’

Those words of top Japanese ace Hiroyoshi Nishizawa, part of a November 1942 conversation that was reported in fighter pilot Saburo Sakai’s autobiography, Samurai, might be the best tribute ever paid to the Grumman F4F Wildcat. While the newer Vought F4U Corsairs and F6F Hellcats grabbed the spotlight, it was the Wildcat that served as the U.S. Navy’s front-line fighter throughout the early World War II crises of 1942 and early 1943.

The Wildcat is unique among World War II aircraft in that it was originally conceived as a biplane. By 1936, the Navy had drawn up specifications for its next generation of shipboard fighters. Although presented with ample evidence that the era of the biplane was over, a strong traditionalist faction within the Navy still felt the monoplane was unsuitable for aircraft carrier use.

As a result, on March 2, 1936, Grumman was ordered to develop yet another single-seat biplane, the G-16, to replace the successful F3F biplane series. The design, the XF4F-1, was ordered both to placate the traditionalists and to be a backup for the Navy’s first monoplane, the Brewster F2A Buffalo. Grumman engineers, however, showed that the installation of a larger engine in the F3F would result in performance comparable to that expected from the new design, and began work on a parallel monoplane project, the G-18 (or XF4F-2). The Navy finally saw the logic of Grumman’s actions and officially sanctioned them.

Although redesigned as a monoplane, the XF4F-2 that rolled out of Grumman’s Bethpage, Long Island, assembly shed on September 2, 1937, showed a strong family resemblance to the F3F family with narrow-track landing gear that retracted upward and inward into the barrel-shaped fuselage. That, in combination with the placement of the cockpit high on the fuselage to give good vision, helped give the Wildcat its distinctive, pugnacious appearance.

Although the new ship was not a true ‘aerobatic’ performer, it was stable and easy to fly and displayed excellent deck-handling qualities. One problem that would remain with the F4F throughout its life, however, was its manual landing gear retraction mechanism. The gear required 30 turns with a hand crank to retract, and a slip of the hand off the crank could result in a serious wrist injury.

The prototype F4F had to best two competitors during spring 1938 trials before its acceptance by the U.S. Navy–the prototype F2A and a naval version of the Seversky P-35. Although the F2A was judged the winner because of teething problems encountered with the F4F, the Navy saw enough potential in the design to order continued development incorporating a newly designed Pratt & Whitney R-1830 radial engine with a two-speed supercharger.

The resulting redesign, the XF4F-3, differed from the original in several respects. Longer-span wings with squared tips–later a Grumman trademark–were added, and the armament of four .50-caliber machine guns was concentrated in the wings. Weight, however, had crept up to 3 tons. First flight for the new machine was February 1939, about two months after the first flight of the Mitsubishi A6M1 Zero prototype in Japan.

International tensions were rising, and the Navy awarded Grumman a contract for 600 Wildcats by the close of 1940. Enough of them were received to begin operations from the carriers Ranger and Wasp by February 1941.

First combat for the F4F was not with the U.S. Navy but with Britain’s Royal Navy, and its first victim was German. The British had shown great interest in the Wildcat as a replacement for the Gloster Sea Gladiator, and the first were delivered in late 1940. On Christmas Day 1940, one of them intercepted and shot down a Junkers Ju-88 bomber over the big Scapa Flow naval base. The Martlet, as the British also called it, saw further action when 30 originally bound for Greece were diverted to the Royal Navy following the collapse of Greece and were used in a ground attack role in the North African Desert throughout 1941.

The Wildcat’s American combat career got off to a more inauspicious start. Eleven of them were caught on the ground during the December 7, 1941, Pearl Harbor attack, and nearly all were destroyed. It was with Marine squadron VMF-211 at Wake Island that the Wildcat first displayed the tenacity that would bedevil the Japanese again and again. As at Pearl Harbor, the initial Japanese attacks left seven of 12 F4F3s wrecked on the field. But the survivors fought on for nearly two weeks, and on December 11, Captain Henry Elrod bombed and sank the destroyer Kisaragi and helped repel the Japanese invasion force. Only two Wildcats were left on December 23, but the pair managed to shoot down a Zero and a bomber before being overwhelmed.

Carrier-based F4F3s engaged the enemy soon after. On February 20, 1942, Lexington came under attack from a large force of Mitsubishi G4M1 Betty bombers while approaching the Japanese base at Rabaul. The F4F fighter screen swarmed over the unescorted bombers, and Lieutenant Edward H. ‘Butch’ O’Hare shot down five of them. He was awarded the Medal of Honor and became the first Wildcat ace.

During the Coral Sea battle in May, F4Fs from the carriers Lexington and Yorktown inflicted heavy losses on the air groups from Shokaku, Zuikaku and Shoho but could not prevent the sinking of Lexington. While the air battles were by no means one-sided, they were clearly a shock to many Zero pilots, who had faced little serious opposition up to that time.

By the time of the Midway engagement in June, the fixed-wing F4F-3 had been replaced by the folding-wing F4F-4. Although the new wings enabled the carriers to increase their fighter complement from 18 to 27, the F4F-4’s folding mechanism, coupled with the addition of two more machine guns, raised its weight by nearly 800 pounds and caused a falloff in climb and maneuverability.

Nearly 85 Wildcats flew from Yorktown, Enterprise and Hornet during Midway, but it was the Douglas SBD Dauntless dive bomber that was destined to be the hero of the battle, sinking the carriers Akagi, Kaga, Hiryu and Soryu, and dealing the Imperial Navy a disastrous defeat.

When news of the U.S. invasion of Guadalcanal reached the Japanese on August 7, 1942, they launched airstrikes from Rabaul. Flying escort was the elite Tainan Kokutai (air group), which counted among its pilots Sakai (64 victories), Nishizawa (credited with 87 before his death in October 1944) and other leading aces. But over Guadalcanal, the Zeros were off-balance from the start. Their first glimpse of the new enemy came when Wildcats of Saratoga‘s VF-5 dived into their formation and scattered it.

Sakai and Nishizawa recovered and claimed eight Wildcats and a Dauntless between them, but they were the only pilots to score. The Navy F4Fs, in return, brought down 14 bombers and two Zeros.

Although exact Japanese losses over Guadalcanal are not known, they lost approximately 650 aircraft between August and November 1942–and an irreplaceable number of trained, veteran airmen. It is certain that the F4Fs were responsible for most of those losses. During the Battle of Santa Cruz on October 26, 1942, Stanley W. ‘Swede’ Vejtasa of VF-10 from the carrier Enterprise downed seven Japanese planes in one fight. Marine pilot Joe Foss racked up 23 of his 26 kills over Guadalcanal John L. Smith was close behind with 19 and Marion Carl, Richard Galer and Joe Bauer were among other top Marine aces.

A large part of the Wildcat success was tactics. The agile Zero, like most Japanese army and navy fighter craft, had been designed to excel in slow-speed maneuvers. U.S. Navy aviators realized early on that the Zero’s controls became heavy at high speeds and were less effective in high-speed rolls and dives. Navy tacticians like James Flatley and James Thach preached that the important thing was to maintain speed–whenever possible–no matter what the Zero did. Although the Wildcat was not especially fast, its two-speed supercharger enabled it to perform well at high altitudes, something that the Bell P-39 and Curtiss P-40 could not do.

The F4F was so rugged that terminal dive airspeed was not redlined. The A6M2’s 7.7mm cowl guns and slow-firing 20mm cannons were effective against an F4F only at point-blank range. But F4F pilots reported that hits from their .50-caliber wing guns usually caused complete disintegration of a Zero.

The Zero and Wildcat shared one serious liability, though. Neither could be modified successfully to keep pace with wartime fighter development. It was determined that the F4F airframe could not accommodate a larger engine without an almost complete redesign, which ultimately did take shape as the new 2,000-hp F6F Hellcat.

The Wildcat’s air combat role began to wane when the Chance-Vought F4U Corsair arrived at Guadalcanal in February 1943. Nevertheless, the stalwart F4F was still the front-line fighter when Admiral Isoroku Yamamoto launched Operation I-Go against Allied forces in the Solomons in April, and Marine Lieutenant James Swett shot down seven (and possibly eight) Aichi D3A1 Val dive bombers in a single combat.

As 1943 wore on, the Wildcat gradually was relegated to a support role as the F6F replaced it aboard fleet carriers. The F4F’s small size, ruggedness and range–enhanced by two 58-gallon drop tanks–continued to make it ideal for use off small escort carrier decks. The little warrior–in both U.S. and Royal Navy markings–contributed to eliminating the U-boat menace in the Atlantic.

General Motors/Eastern Aircraft produced 5,280 Wildcats like this FM-2. The fighter was optimized for smaller escort carriers, with a more powerful engine, and a taller tail to cope with the torque.

A General Motors­built version of the F4F received a marginal boost when a Wright 1,350-hp single-row radial was installed in place of the 1,200-hp Pratt & Whitney. The first production models of the new variant, designated the FM-2, arrived in late 1943. The FM-2’s new engine, coupled with a 350-pound weight reduction, produced improvements in performance over the F4F. In fact, postwar tests revealed the late-model A6M5 Zero to be only 13 mph faster.

FM-2s were normally teamed with TBF Avengers in so-called VC ‘composite’ squadrons on small escort carriers. During the Battle of Samar on October 25, 1944, FM-2s and Avengers from several ‘baby flattops’ aided destroyers in disrupting an overwhelming Japanese battleship task force that surprised the American invasion fleet off the Philippines. The aircraft, although handicapped by a lack of anti-shipping ordnance, so demoralized the Japanese that a potential American disaster was averted.

Although opportunities for air combat were few, FM-2s notched a respectable 422 kills–many of them kamikaze aircraft–by the end of the war. On August 5, 1945, a VC-98 FM-2 from USS Lunga Point shot down a Yokosuka P1Y1 Frances recon bomber to score the last Wildcat kill of the war.

In terms of sheer numbers, the F4F’s kill tally was less than the Corsair and much less than the Hellcat. But the Hellcat did not appear until the really critical combats were long over it was the underdog F4F, flown by highly skilled U.S. Navy and Marine pilots, that provided the few sparks of victory early in the war, when the Japanese onslaught in the Pacific seemed overwhelming.

Many aircraft achieved greatness during World War II, but few could be called heroic. The F4F Wildcat, usually outnumbered and outclassed by its opponents, was a heroic airplane.

This article was written by Bruce L. Crawford and originally published in Aviation History. For more great articles subscribe to Aviation History magazine today!

Wild Cat II Sch - History

The Steiger 4wd emerged from the Red River Valley region nearly 50 years ago. Brothers, Doug and Maurice Steiger, built the first Steiger in their Thief River Falls, Minnesota dairy barn, during the winter of 1957-58. Steiger #1 was built from truck components and powered by a 238 hp Detroit Diesel Engine. The simple and powerful design impressed local farmers and soon the Steiger brothers were building tractors.

The Steiger 4wds expanded in 1963 to include a horse power range from 118 hp to 300 hp. They stood out with the Steiger name plate cut from 3/8-inch steal and the models V-8 engine designation cut as a large V in the tractors grill. The success of the Steiger is the main feature was standard components. Major parts, such as engines, transmissions and power trains were outsourced from brand name suppliers like Caterpillar, Cummins, Allison, Clark and Spicer. Farmers liked the components because could find replacement parts nation wide.

By the 1970s Steiger 4wds were being sold nation wide. Grain, vegetable, row crop and dairy farms were all finding uses for the big 4wds. Steiger 4wds were rolling out of a large factory in Fargo, North Dakota. Cat names like Wildcat, Bearcat, Cougar, Panther and Tiger donated the horse power ranges. New styling and power lead Steiger to the top of the pack with a 36% market share.

As the Steiger Tractor company entered the 1980s, the tractors size and popularity had grown beyond anything the Steiger brothers would have imagined in 1958. In 1983 Steiger introduced its largest tractor the 525 hp KP-525 and ultra modern Panther 1000 series. The 1000 series was a new 4wd from the ground up. The cab offered an unmatched view of the field and the new sleek hood design allowed for a clear line of site for the ground ahead. By 1985 Steiger was producing 26 tractor models with three engine options, a horse power range from 190 hp for row crop farmers up to 525 hp for the ultimate plowing power.

Steiger in a little over 20 years had become a legend in farming. Before Steiger, most farmers beyond the parries could not imagine using an articulated tractor in their operation. Steigers range of model sizes, horse power, transmissions and treads took 4wd power coast to coast. The Iowa corn farmer, California vegetable farmer, Kansas wheat farmer, Arkansas rice farmer, Louisiana sugar can plantation, Texas rancher and Wisconsin dairy farmer all found a way to incorporate 4wd power. Steiger 4wds were also a global tractor with models going to Europe, Africa and Australia.

The Steiger Tractor Company was unmatched in 4wd choices. Unfortunately the economy of the 1980s did not allow farmers to afford so many tractor options in the high horse power class. Sales dropped off and the Steiger factory was only producing at a quarter of its capacity. In 1986 Steiger Tractor Company was purchased by Tenneco the parent company of Case. Case continued producing green Steigers as well as the new 9100 series Case International Steigers. The Steiger name appeared on green and red tractors until 1989.

Today the CaseIH STX Steiger series is the market leader in 4wds, with models ranging from 275-500 hp. The classic green Steigers still account for a large portion of 4wds used in farming. The Barn Series, Series I, Series II, Series III and 1000 Series were built to last a life time. Many have 10,000, 15,000 and 20,000+ and are running as well as the day they rolled out of the factory. Farmers like Steiger 4wds because they are easy to maintain and use. They represent power to get across the field and put the crop in quickly.

The Steiger 4wd history below is a general overview of the Steiger Tractor Company's heritage from 1958-1989. This section highlights the general history, models and horse power ranges of the Barn Series, Series I, Series II, Series III, Series IV, 1000 Series and 9100 Series Steigers.

Years of Production: 1986-1989

Models: 9110 (190 hp), 9130 (235 hp), 9150 (280 hp), 9170 (335 hp), 9180 (375 hp), 9190 (525 hp)

History: The poor farm economy took its tool on the Steiger Tractor Company. With the world farm economy struggling, Steiger sold fewer tractors. In 1986, with the plant operating at 25% of capacity, Steiger filed for Chapter 11 bankruptcy protection. Later that year, Tenneco, Inc. the then parent of J.I. Case, bought Steiger. In 1985 Tenneco purchased Interational Harvesters Ag Division and formed Case-International under the J.I. Case Company. Case-IH tractors took on International's famous Harvester red. With the purchase of Steiger, Case continued to produce articulated 4wds under the Steiger name as well as producing the first red Case International 9100 series 4wds. Under Case-IH the Cat names were replaced with numbers: Puma = 9110, Wildcat = 9130, Cougar = 9150, Panther = 9170, Lion = 9180, Tiger = 9190. From 1986-1989 customers could purchase a red 9100 series Steiger. In 1990, Case-IH introduced the 9200 series and phased out the Steiger name. Case returned the Steiger name to the 4wd in 1995 with the 9300 series. The Steiger name plate badge was placed on the grill and the CaseIH name on the hood decal. Today the CaseIH STX Steiger series leads the 4wd market in sales and continues the solid Steiger tradition started in 1958.

Years of Production: 1983-1986

Models: Puma (190 hp) ,Wildcat (220 hp), Cougar ( 225 hp) CR-1225, KR-1225, Bearcat (235 hp), Cougar (280 hp), Panther (325/360/400 hp) CP-1325, KP-1325, CP-1360, KP-1360, CP-1400, KP-1400, Panther (335 hp), Lion (375 hp).

History: A new style of Steiger tractor was released in 1983 along with the series IV. The 1000 series was launched with six new Panther models. The Panther 1000 models offered a 12-speed full powershift transmission, on-board computer, and new Safari Cab and sloped to improve visibility. The Panther 1000 series was produced along side the series IV models through 1985. The initial Panther 1000 models were ranged from 325-400 hp and were powered by Caterpillar or Cummins engines. Steiger used CP to mark the Caterpillar engine Panthers and KP for the Cummins models. In 1985 Steiger introduced the Cougar 1000 with two 225 hp models. CR was the Caterpillar model and KR was the Cummins Cougar 1000. Between 1983 and 1985 Steiger was producing 26 different tractors with the Series IV models and the Panther and Cougar 1000 models. In 1986 Steiger revamped the entire line and simplified it to 6 models. The 1000 series accounted for five models. The new Puma and Wildcat 1000 tractors offered row crop farmers a new modern 4wd. The Bearcat and Cougar 1000 tractors supplied mid-range power. The 6 Panther models were narrowed down to one 335 hp tractor. The new Lion 1000 topped of the series at 375 hp.

Years of Production: 1983-1985 *

Models: Bearcat (225 hp) CM-225, KM-225, Cougar (250/280 hp) CM-250, KM-250, CM-280, KM-280, CS-280, KS-280, Panther (325/360 hp) CM-325, KM-325, SM-325, SM-325, CS-325, KS-325, CM-360, KM-360, CS-360, KS-360, Tiger (525 hp) KP-525. ( * The Tiger IV was produced from 1984-1988 and ended production as the Case International 9190 )

History: The Series IV Steiger 4wds were best of the line that started in 1969 with the Wildcat I. All of the possible refinements and upgrades had been made. Identification numbers changed on the Series IV. Caterpillar, Cummins and Komatsu engines were the Series IV power plants. The Series IV Bearcat and Cougar were powered by either Caterpillar or Cummins engines. Designation C was for Caterpillar and K for Cummins. The mid-range Panther IV had three engine options, a Caterpillar 3406, Cummins NT 855 or new Komatsu SA6D-125. The Panther IV had a power range of 325 to 360 hp. S designated the Komatsu engine option. The Tiger IV is the largest Steiger built to date at 525 hp (the CaseIH Steiger STX 500 at 500 hp is catching up). The Tiger IV was powered by a Cummins KTA 1150. There were two types transmissions for the series IV. M denoted the 20 speed manual 4wds and S was for the Steigermatic transmission. The Tiger IV was designated KP for the Cummins engine and powershift transmission.

Years of Production: 1982-1984

Models: Model CA or CU 280 (280 hp), Model CA or CU 325 or 360 (325/360 hp)

History: In 1982 Steiger released a range of yellow tractors for industrial applications in construction, mining, forestry and land leveling. The Industrial tractors were based on the PTA Cougar and Panther design. Steiger beefed up the axles, transmission and hydraulic flow on the Industrial models. The model numbers indicate the engine and horse power. Cummins powered the CU-280, CU-325 and CU-360. The CA-280, CA-325 and CA-360 used Caterpillar engines. Steiger also offered Agricultural models of the CA and CU models for farming. The extra hydraulic power was well matched for large plows, discs and field cultivators.

Years of Production: FW Series 1978-1982

Models: FW 20 (210 hp) FW 30, (270 hp) FW 40 (295 hp) FW 60 (360 hp). FW 20 = Bearcat FW 30 = Cougar FW 40 = Cougar Fw 60 = Panther

Years of Production: PT Series 1977-1981/PTA Series 1978-1982

Models: PT Bearcat (225 hp) PT-220, Cougar (250/270 hp) PT-250, PT-270, Panther (350 hp) PT-350. PTA Cougar (251/270/280 hp) PTA-251, PTA-270, PTA-280, Panther (296/297/310/325 hp) PTA-296, PTA-297, PTA-310, PTA-325.

History: 1977 brought additional advancement to the Steiger Series III with the introduction of electronically controlled PTOs. The Bearcat, Cougar and Panther were available with a limited 125 hp pto. The PT prefix denoted the pto models. The PT Steigers have a longer hood with a slight arch in the center.

In 1980 Steiger introduced an automatic transmission series fitted with an electronically controlled pto, called PTA. Cougar and Panther tractors were equipped with the new feature. For example the PTA-325 Panther with Steiger-Matic assesses speed and load factors all by itself, automatically maintaining the best gear for maximum power and efficiency. In fact, Steiger-Matic actually locks into each gear to provide a direct link between engine and axel, which gives the operator the efficiency of manual transmission plus the convince of an automatic. The Steiger's Caterpillar powered Panther was the heavy hitter of the Steiger PTA line. As a fully automatic model it proved to be a and still is one of the most popular Steigers.

Years of Production: 1976-1983

Models: Wildcat (200 hp) ST-200, RC-200, Bearcat (220/225 hp) ST-220, ST-225, Cougar (250/251/270/280 hp) ST-250, ST-251, ST-270, ST-280, Panther (310/320/325/350 hp) ST-310, ST-320, ST-325, ST-350, Tiger (450/470 hp) ST-450, ST-470.

History: 1976 ushered in a new generation of Steiger 4wds. The Series III Steigers were introduced to dealers at the winter meeting in Florida. A Circus theme was used complete with a lion tamer. As the new tractor models were announced the lion tamer cracked his whip and the new Wildcat, Bearcat, Cougar and Panther rolled out into the ring. These new models offered both Caterpillar and Cummins engines with a 10 speed constant mesh transmission. The big change from Series II was the all new Safari cab. The Safari offered a new level of comfort and quite with easy to reach controls and improved visibility. The Series I and II Steigers shift was in the center of the cab and the hydrualic switch on the rear of the cab. The Series III cab made operating the 4wd convenient and allowed the operator to sit in air conditioning and the power do the work. In 1977 Steiger increased the series power to include the 450 and 470 hp Tiger models. The Series III Steiger 4wds captured 36% of the North American 4wd market.

Years of Production: 1974-1976

Models: Super Wildcat (200 hp) ST-200, RC-200, Bearcat (225 hp) ST-225, RC-225, Cougar (300 hp) ST-300, Panther (310 hp) ST-310, Turbo Tiger (320 hp) ST-320.

History: In 1974 Steiger broke ground on a new factory. In less than a year the new 420,000 square foot manufacturing facility was finished. It employed 1,100 people and could produce a new Steiger 4wd every 18 minutes. This plant is owned by Case-New Holland today and produces the CaseIH STX Steiger 4wd line, Case/New Holland Wheel Loaders, the New Holland TJ 4wd line and TV 145 bi-directional tractor. In 1974 the new Fargo plant began producing the Steiger Series II 4wds. Steiger Series II 4wds were basically the same in as far as tin work and features. Steiger changed the paint scheme from green and red to a green frame and wheels and a black grill, hood and cab. The CAT engine was also painted black. The Panther was added to the line. Steiger also began offering the Wildcat and Bearcat available in standard and row crop. The Series II Steigers were denoted with the prefix ST for standard models and RC for row crop models in front of the horse power. For example the Panther II was the ST-310 (Standard 310 hp) and the Bearcat II could be the ST-225 (Standard 225 hp) or RC-225 ( Row Crop 225 hp).

Years of Production: 1969-1974

Models: Wildcat (175 hp), Super Wildcat (200 hp), Bearcat (225 hp), Cougar (300 hp), Tiger (310 hp), Turbo Tiger (320 hp).

History: The Steiger brand 4wds quickly grew in popularity with farmers in the plains. Selling 4wds beyond that region, proved to be difficult. Salesman Earl Christianson saw 200 hp machines working on construction sites and watched 90 hp-50 hp 2wd tractors struggling n farmland. Why not big horse power on the farm? Earl joined the Steiger brothers in the 1960s and greatly expanded their sales region. Steiger grew beyond the barn and an investor group purchased the company to expand and improve its product range. In 1969 Steiger opened a new production facility in Fargo, North Dakota. The Wildcat was the first Steiger to roll out of the factory. Steiger replaced the numbered models with the famous cat names that marked the 4wd line horse power range for two decades. The Series I Steigers offered a new refined chassis, tin work, a climatized cab mounted independently from the tractor frame and a 10/2 transmission. The Series I tractors continued using Steiger green on the frame and red on the grill and wheels. All of the tractors used Caterpillar engines and they were left in standard CAT yellow. In 1970 sixty-six dealerships took on Steiger. Series I Steigers were sold in new markets from coast to coast. In the South to rice farmers in Arkansas, Louisiana and Oklahoma were quick to add 4wds to their operation. On the East Coast in New York, Pennsylvania, Maryland, Delaware and North Carolina cash crop and dairy farmers used Steigers to plow their land like never before. On the West Coast large vegetable farmers in California, grass seed farmers in Oregon and hillside wheat farmers in Washington added the 4wds to their operations.

Years of Production: 1963-1969

Models: 1250 (150 hp), 1700 (216 hp), 2200 (238 hp) 3300 (328 hp) 800 Tiger (300 hp).

Common Cat Diseases

As a cat parent, it is important to recognize the signs and symptoms of common illnesses so you can seek veterinary help for your feline friend in a timely manner if necessary. Read on for information about diseases and other medical inflictions that frequently impact cats.


Cancer is a class of diseases in which cells grow uncontrollably, invade surrounding tissue and may spread to other areas of the body. As with people, cats can get various kinds of cancer. The disease can be localized (confined to one area, like a tumor) or generalized (spread throughout the body).

Causes of Cancer

Cancer is a “multifactorial” disease, which means it has no known single cause. However, we do know that both hereditary and environmental factors can lead to the development of cancer in cats.

  • Squamous cell carcinoma of the ear, eyelid or nose is a skin cancer caused by repeated exposure to the sun. White, or light colored, cats are more susceptible to squamous cell carcinoma.
  • Lymphosarcoma or lymphoma (LSA), is one of the most common type of cancer in cats. Some reports estimate that 30% of all reported cat cancers are due to LSA. Feline leukemia virus (FeLV) is linked to most forms of LSA except for the gastrointestinal (GI) form. FeLV is a transmittable retrovirus that can be passed in utero as well as through saliva and direct contact. Primarily a disease in younger cats, the virus doesn’t always manifest symptoms, so it is important to have your cat tested regularly to prevent transmission and progression. There is a vaccine available for FeLV that your veterinarian can discuss with you based on your cat’s lifestyle and risk of exposure to FeLV.

The GI form of LSA (the most common form) can cause a large mass in the stomach or intestine or diffuse infiltration throughout the intestinal tract.

It is important to take your cat to your veterinarian if any evidence of disease is noted. LSA is not curable, however, most cats respond well to treatment.

Cancer Symptoms

Symptoms of cancer in cats may include:

  • Lumps (which are not always malignant, but are always worth having a veterinarian examine)
  • Swelling
  • Persistent sores or skin infections
  • Abnormal discharge from any part of the body
  • Bad breath
  • Listlessness, lethargy or other marked change in behavior
  • Weight loss
  • Sudden lameness
  • Diarrhea or vomiting
  • Scaly and/or red skin patches
  • Decreased or loss of appetite
  • Difficulty breathing, urinating or defecating
  • Change in behavior

Diagnosing Cancer in Cats

  • If a lump is present, the first step is typically a needle biopsy, which removes a very small tissue sample for microscopic examination of cells. Alternately, surgery may be performed to remove all or part of the lump for diagnosis by a pathologist.
  • Radiographs, ultrasound, blood evaluation and other diagnostic tests may also be helpful in determining if cancer is present or if it has spread.

Cats More Prone to Cancer

  • Though cancer can be diagnosed in cats of all ages and breeds, it is much more common in older cats.
  • Certain breeds are prone to specific cancers, but cats with white ears and heads are particularly susceptible to skin cancer.

Ask your vet if your cat falls into specific at-risk categories.

Cancer Prevention

  • Keeping your cat indoors will protect her from certain skin cancers caused by repeated sun exposure and sunburn.
  • Breast cancer is a common cancer for cats, but it can be avoided by having your cat spayed before her first heat cycle.

Cancer Treatments

  • Treatment options vary and depend on the type and stage of cancer.
  • Common treatments include surgery, chemotherapy, radiation and immunotherapy or a combination of therapies. Success of treatment depends on the form and extent of the cancer and the aggressiveness of the therapy. Of course, early detection is best.
  • Some cat owners opt for no treatment of the cancer, in which case palliative care, including pain relief, should be considered. Regardless of how you proceed after a diagnosis of cancer in your pet, it is very important to consider his quality of life when making future decisions.
  • Some cancers can be cured, and almost all patients can receive at least some benefit from treatment. Please note that if your cat’s cancer is not curable, there are still many things you can do to make your pet feel better. Don’t hesitate to talk to your vet about your options. And remember good nutrition and loving care can greatly enhance your cat’s quality of life.

Knowing When to Consult Your Vet

Contact your veterinarian immediately if your cat shows any of the clinical signs mentioned on the list above. Should your cat receive a diagnosis of cancer, you may wish to consult a veterinary oncologist, often employed by specialty veterinary practices and teaching hospitals.


Diabetes in cats is a complex disease caused by either a lack of the hormone insulin or an inadequate response to insulin. After a cat eats, her digestive system breaks food into various components, including glucose—which is carried into her cells by insulin. When a cat does not produce insulin or cannot utilize it normally, her blood sugar levels elevate. The result is hyperglycemia, which, if left untreated, can cause many complicated health problems for a cat.

It is important to understand that diabetes is considered a manageable disorder—and many diabetic cats can lead happy, healthy lives. Some may even go into remission!

Diabetes can be classified as:

  • Type I (lack of insulin production)
  • Type II (impaired insulin production along with an inadequate response to the hormone).

Cats with type II diabetes can progress to type I diabetes. In fact, by the time most cats are diagnosed with diabetes, they are identified as having the type I disorder. These cats require insulin therapy for survival. Cats with type II disease may respond to other forms of therapy.

Diabetes Symptoms in Cats

The following are signs that your cat may be diabetic:

  • Change in appetite (either increased or decreased)
  • Weight loss
  • Excessive thirst/increase in water consumption
  • Increased urination
  • Urinating in areas other than litter box
  • Unusually sweet-smelling breath
  • Lethargy
  • Dehydration
  • Unkempt hair coat
  • Urinary tract infection

Causes of Diabetes

The exact cause of diabetes is unknown. Genetics, pancreatic disease, certain medications and abnormal protein deposits in the pancreas can play a role in causing this disorder.

The most important factors in the development of diabetes seem to be obesity, gender (male cats are more commonly afflicted than females) and age.

Diagnosing Diabetes

To properly diagnose diabetes, your veterinarian will collect information about clinical signs, perform a physical examination and check blood work and urinalysis.

Treating Diabetes

  • Every diabetic cat is an individual and will respond differently to therapy. Diabetes treatment is based on how severe the signs of disease are and whether there are any other health issues that could complicate therapy.
  • Some cats are seriously ill when first diagnosed and require intensive hospitalized care for several days to regulate their blood sugar levels.
  • Cats who are more stable when first diagnosed may respond to oral medication or a high-fiber diet.
  • For most cats, insulin injections are necessary for adequate regulation of blood glucose. Once your pet’s individual insulin treatment is established, typically based on weight, you will be shown how to give him his insulin injections at home.
  • Your vet may also show you how to perform glucose tests at home. Other routine blood work may also be necessary.

As your veterinarian will explain, it’s important to always give your cat insulin at the same time every day and feed her regular meals in conjunction with her medication this allows increased nutrients in the blood to coincide with peak insulin level. This will lessen the chance that her sugar levels will swing either too high or too low. You can work with your vet to create a feeding schedule around your pet’s medication time. It is also important to avoid feeding your diabetic cat treats that are high in glucose.

Diabetes Prevention

A proper diet and regular exercise can go a long way to avoid the development of feline diabetes. Aside from other negative effects, obesity is known to contribute to insulin resistance.

If You Suspect Your Cat Has Diabetes

If your cat is showing any abnormal clinical signs as listed above, make an appointment to see your veterinarian immediately. If a diabetic cat is not treated, he can develop kidney disease, neurological disorders or other metabolic diseases. Cats with type I diabetes require insulin therapy for survival.

Feline Immunodeficiency Virus (FIV)

Cats infected with feline immunodeficiency virus (FIV) may not show symptoms until years after the initial infection occurred. Although the virus is slow-acting, a cat’s immune system is severely weakened once the disease takes hold. This makes the cat susceptible to various secondary infections. Infected cats receiving supportive medical care and kept in a stress-free, indoor environment can live relatively comfortable lives for months to years before the disease reaches its chronic stages.

An FIV-infected cat may not show any symptoms for years. Once symptoms do develop, however, they may continually progress—or a cat may show signs of sickness interspersed with health for years. If your cat is demonstrating any of the following symptoms, please have examined by your veterinarian:

  • Enlarged lymph nodes
  • Fever
  • Anemia
  • Weight loss
  • Disheveled coat
  • Poor appetite
  • Diarrhea
  • Abnormal appearance or inflammation of the eye (conjunctivitis)
  • Inflammation of the gums (gingivitis)
  • Inflammation of the mouth (stomatitis)
  • Dental disease
  • Skin redness or hair loss
  • Wounds that don’t heal
  • Sneezing
  • Discharge from eyes or nose
  • Frequent urination, straining to urinate or urinating outside of litter box
  • Behavior change

FIV Transmission

  • FIV is mainly passed from cat to cat through deep bite wounds, the kind that usually occur outdoors during aggressive fights and territorial disputes—a perfect reason to keep your cat inside.
  • Another, less common mode of transmission is from an FIV-infected mother cat to her kitten. FIV does not seem to be commonly spread through sharing food bowls and litter boxes, social grooming, sneezing and other casual modes of contact.
  • Although any feline is susceptible, free-roaming, outdoor intact male cats who fight most frequently contract the disease. Cats who live indoors are the least likely to be infected.

Please note: FIV cannot be transmitted from cat to human, only from cat to cat.

Preventing FIV

  • The best way to prevent your cat from contracting the virus is to keep him indoors, avoiding any chance of contact with infected felines.
  • If you walk your cat, keep him on a leash when outdoors.
  • If your cat is going to be spending any time in a cattery or in a home with other felines, make sure all cats have tested negative for FIV.
  • Any recently adopted cat should be tested for FIV prior to entering your home.
  • You may also want to speak to your veterinarian about the FIV vaccine and if it is appropriate for your cat.

When to Consult Your Veterinarian

If you suspect your cat has FIV, have him examined and tested by your veterinarian right away. During your visit, be ready to describe any symptoms that you have detected, no matter how minute they seem. Also make sure to keep your cat indoors, away from other felines who might possibly be infected or whom he could infect, until you have a diagnosis.

Without proper treatment, the secondary infections that can occur as a consequence of FIV can progress to life-threatening conditions. Additionally, cats with FIV can develop various forms of cancer, blood diseases or kidney failure, which will ultimately claim the cat’s life.

Diagnosing FIV

  • FIV infection is routinely diagnosed by blood testing.
  • The FIV status of every cat should be known.
  • The most common type of test looks for the presence of antibodies to the virus in the blood. No test is 100% accurate all of the time, and your veterinarian will interpret the test result and determine whether further testing is needed to confirm either a positive or negative test result. Once a cat is determined to be FIV-positive, that cat is capable of transmitting the disease to other cats.
  • Since it is possible for an infected mother cat to transfer FIV antibodies to her kittens, these kittens may test positive from their mother’s antibodies until they have cleared them from their systems, which happens by six months of age. Kittens who test positive for FIV antibodies when they’re younger than six months should undergo antibody tests again at a later date to see if they are infected.

FIV Treatment

Unfortunately, there is no specific antiviral treatment for FIV. Cats can carry the virus for a long time before symptoms appear. Therefore, treatment focuses mainly on extending the asymptomatic period or, if symptoms have set in, on easing the secondary effects of the virus. Your veterinarian may prescribe some of the following treatments:

  • Medication for secondary infections
  • Healthy, palatable diet to encourage good nutrition
  • Fluid and electrolyte replacement therapy
  • Anti-inflammatory drugs
  • Immune-enhancing drugs
  • Parasite control

Caring for an FIV-Infected Cat

  • Keep your cat indoors. This will protect him from contact with disease-causing agents to which he may be susceptible. By bringing your cat indoors, you’re also protecting the uninfected cats in your community.
  • Watch for changes—even seemingly minor—in your cat’s health and behavior. Immediately report any health concerns to your vet.
  • Bring your cat to your vet at least twice per year for a wellness checkup, blood count and urine analysis.
  • Feed your cat nutritionally balanced food—no raw food diets, please, as bacteria and parasites in uncooked meat and eggs can be dangerous to immunocompromised pets.
  • Be sure your cat is spayed or neutered.

Feline Leukemia Virus (FelV)

First discovered in the 1960s, feline leukemia virus is a transmittable RNA retrovirus that can severely inhibit a cat’s immune system. It is one of the most commonly diagnosed causes of disease and death in domestic cats. Because the virus doesn’t always manifest symptoms right away, any new cat entering a household—and any sick cat—should be tested for FeLV.

FeLV weakens an animal’s immune system and predisposes cats to a variety of infections and diseases, including anemia, kidney disease and lymphosarcoma, a highly malignant and fatal cancer of the lymph system.

Young kittens and cats less than one year of age are most susceptible to the virus. Cats living with an infected cat, allowed outdoors where they may be bitten by an infected cat, and kittens born to a mother who is FeLV positive are most at risk for infection.

  • The FeLV virus is shed in many bodily fluids, including saliva, nasal secretions, urine, feces and blood.
  • FeLV is most commonly transmitted through direct contact, mutual grooming and through sharing litter boxes, food and water bowls.
  • It can also be passed in utero or through mother’s milk.
  • Infected outdoor cats fighting with other cats can transmit the disease through bites and scratches.

Healthy cats over three months of age and vaccinated for FeLV are highly unlikely to contract the virus from another cat.

Signs of FeLV

Cats can be infected and show no signs. Others may exhibit:

  • Loss of appetite and weight loss
  • Pale or inflamed gums
  • Poor coat condition
  • Abcesses
  • Fever
  • Upper respiratory infections
  • Diarrhea and vomiting
  • Seizures
  • Changes in behavior
  • Vision or other eye problems
  • Enlarged lymph nodes
  • Reproductive problems (in females)
  • Jaundice
  • Chronic skin disease
  • Respiratory distress
  • Lethargy

Preventing FelV

  • There is a vaccine available for cats who are at risk of contracting FeLV. Like all vaccines, there are risks involved in vaccination, and the vaccine is not a 100% guarantee against infection. Your veterinarian can best evaluate whether this vaccine is right for your cat.
  • As with any infectious disease, the best prevention is eliminating sources of exposure. Routine FeLV testing and keeping your cat indoors and away from cats whose FeLV status is not known remain the best way to prevent your cat from becoming infected.

Diagnosing FelV

There are several types of tests available to diagnose FeLV.

  • Most veterinarians and shelter professionals use the ELISA (enzyme-linked immunosorbent assay) test, which detects antigen to the FELV virus in the bloodstream.
  • Other tests like the IFA (indirect fluorescent antibody) test or PCR (polymerase chain reaction) test are recommended to confirm positive ELISA test results.

Caring for a Cat with FelV

  • Feed your cat a nutritionally balanced diet, one free of raw meat, eggs and unpasteurized dairy products, which can harbor bacteria and parasites and lead to infection.
  • Provide a quiet place for your cat to rest indoors and away from other cats who could promote disease.
  • Bring your cat to the vet every six months—at the very least—for a wellness checkup and blood tests.
  • During the early stages of infection, a cat may not show any clinical signs, but he can still pass the virus to other cats. It’s not advisable to introduce a new uninfected cat into the household, even one who has been properly vaccinated against FeLV. Those living in close quarters with infected cats are most at risk for infection, and should be tested for the virus and, if negative, be housed separately.
  • FeLV is contagious to other cats, but not to humans or other species. Other cats in the house can acquire the virus from an infected cat. Though the virus doesn’t live long outside of the body, and is easily inactivated with common disinfectants, it can be passed through mutual grooming, shared food and water as well as common litter boxes.
  • Sadly there is no cure for FeLV, and it is estimated that less than 20% of clinically infected cats survive more than three years of active infection. In the case of those cats who develop cancer, chemotherapy can help prolong life, but treatment often focuses on providing the best quality of life.


Spread by infected mosquitoes, heartworm is increasingly being recognized as an underlying cause of health problems in domestic cats. Cats are an atypical host for heartworms. Despite its name, heartworm primarily causes lung disease in cats. It is an important concern for any cat owner living in areas densely populated by mosquitoes, and prevention should be discussed with a veterinarian.

You may have thought heartworm disease only affects dogs, and it’s true that the infection is less common in cats. The cat is not a natural host for the heartworm parasite, Dirofilaria immitis, and so the heartworm is not likely to complete its entire life cycle. That means that fewer and smaller worms survive, and many do not reach a cat’s heart. The worms that do survive—and the resulting immune reaction that the cat’s body sets up to kill the developing worms—can cause severe health problems.

Causes and Signs of Heartworm Disease

When a mosquito carrying the heartworm parasite, Dirofilaria immitis, bites a cat, larvae are transmitted into the bloodstream. The larvae migrate toward the heart over a period of around four to six months, maturing as they go, then settle in the heart, pulmonary arteries and blood vessels of the lungs. Because a domestic cat is not a natural host for the heartworm parasite, many of the worms die. These—along with the living worms—cause severe inflammatory and immune responses in an infected cat.

Cats of all ages, living in any region, can contract heartworm, but the disease is more prevalent in felines who live in areas densely populated by mosquitoes. Outdoor cats are at greater risk because of increased exposure to mosquitoes. However, indoor cats are also susceptible to mosquito bites, so it’s smart to discuss prevention with your vet. The heartworm infection can be especially life-threatening to kittens and older cats.

The following signs may indicate that your cat has been infected:

  • Persistent cough
  • Breathing difficulties (panting, wheezing, rapid or open-mouthed breathing)
  • Depression
  • Loss of appetite
  • Weight loss
  • Sporadic vomiting
  • Lethargy
  • Sudden death

Breathing difficulties that occur in the first stage of heartworm disease, caused by worms newly arriving in the heart and lungs, were likely previously diagnosed as feline asthma or bronchitis. However, these breathing problems are now thought to have actually been due to what is now called heartworm-associated respiratory disease (HARD).

Heartworm Prevention

  • There are several FDA-approved medications available that reliably prevent feline heartworm infection. Check with your vet and please remember, it’s recommended that cats are screened for heartworm infection with blood tests before being given any type of preventative medication.
  • It’s also a good idea to limit your cat’s exposure to mosquito-infested areas and bring her in for preventative screenings during vet visits.
  • Regular checkups are key to detecting early infections and can give your cat a good chance at recovery.

Diagnosing Heartworm Disease

Heartworm disease is not as easily diagnosed in cats as it is in dogs.

  • Routine testing requires a combination of blood tests.
  • When cats show signs of respiratory difficulty and heartworm is suspected, diagnosis is usually based on a cat’s history, physical examination, radiographs, echocardiogram and blood tests.

Treating Heartworm Disease

There are currently no products in the United States approved for treating feline heartworm infection. The good news is that many heartworm-infected cats are able to fight the infection themselves, and can be monitored with radiographs every few months, while waiting out the worms’ lifespan. If an infected cat shows symptoms of lung disease, the cat can be given a cortisone-like medication as needed. Medication can also be given to help control coughing and vomiting.

Although some cats are able to fight the infection on their own, the following can occur if heartworms are not monitored and treated:

  • Damage to walls of heart
  • Damage to pulmonary blood vessels
  • Possible obstruction of blood flow through pulmonary arteries
  • Impaired breathing
  • Heart and lung failure
  • Kidney and liver damage
  • Sudden death

High-Rise Syndrome

Many pet parents eagerly open their windows to enjoy the weather during the summer months. Unfortunately, unscreened windows pose a real danger to cats, who fall out of them so often that the veterinary profession has a name for the complaint—High-Rise Syndrome. Falls can result in shattered jaws, punctured lungs, broken limbs and pelvises—and even death.

  • Cats have excellent survival instincts, and they don’t deliberately “jump” from high places that would be dangerous. Most cats fall accidentally from high-rise windows, terraces or fire escapes.
  • Cats have an incredible ability to focus their attention on whatever interests them. A bird or other animal attraction can be distracting enough to cause them to lose their balance and fall.
  • Because cats have little fear of heights and enjoy perching in high places, pet owners often assume that they can take care of themselves. Although cats can cling to the bark of trees with their claws, other surfaces are much more difficult, such as window ledges, concrete or brick surfaces.
  • When cats fall from high places, they don’t land squarely on their feet. Instead, they land with their feet slightly splayed apart, which can cause severe head and pelvis injuries.
  • It is a misconception that cats won’t be injured if they fall from one- or two-story buildings. They may actually be at greater risk for injury when falling shorter distances than by falling from mid-range or higher altitudes. Shorter distances do not give them enough time to adjust their body posture to fall correctly.
  • When cats fall from high-rise buildings, they may end up on sidewalks or streets that are dangerous and unfamiliar to them. Never assume that the animal has not survived the fall immediately rush the animal to the nearest animal hospital or to your veterinarian.
  • There is a 90% survival rate for cats who are high-rise victims if they receive immediate and proper medical attention.

Preventing High-Rise Syndrome

To keep your cat safe during the summer, take the following precautions:

  • Install snug and sturdy screens in all your windows.
  • If you have adjustable screens, please make sure that they are tightly wedged into window frames.
  • Note that cats can slip through childproof window guards—these don’t provide adequate protection!


Rabies is a viral disease that affects the brain and spinal cord of all mammals, including cats, dogs and humans. This preventable disease has been reported in every state except Hawaii. There’s good reason that the very word “rabies” evokes fear in people—once symptoms appear, rabies is close to 100% fatal.

Rabies Transmission

There are several reported routes of transmission of the rabies virus.

  • Rabies is most often transmitted through a bite from an infected animal.
  • Less frequently, it can be passed on when the saliva of an infected animal enters another animal’s body through mucous membranes or an open, fresh wound.
  • The risk for contracting rabies runs highest if your cat is exposed to wild animals. Outbreaks can occur in populations of wild animals (most often raccoons, bats, skunks and foxes in this country) or in areas where there are significant numbers of unvaccinated, free-roaming dogs and cats.
  • In the United States, rabies is reported in cats more than in any other domestic species.
  • Unvaccinated cats who are allowed to roam outdoors are at the highest risk for rabies infection.
  • Feral cat populations remain a reservoir host for the rabies virus.

Rabies Prevention

  • Vaccination is the key—and in many areas of the country, such as New York City, it's the law.
  • Some local ordinances require lengthy quarantines—or euthanasia—of pets who have bitten someone if their owners do not have proof of current vaccination.
  • Vaccinating your cat doesn't just protect her from rabies—it also protects your cat if she bites someone.
  • In municipalities where rabies vaccinations for cats are not required, the decision to vaccinate is best left to the judgment of the veterinarian and the cat guardian because some cats experience serious side effects to the rabies vaccine.
  • The vaccine should definitely be administered if your cat spends any time outdoors (ASPCA experts recommend keeping pet cats indoors).

Symptoms of Rabies

  • Animals will not show signs immediately following exposure to a rabid animal. Symptoms can be varied and can take months to develop. Classic signs of rabies in cats include:
  • Changes in behavior (including aggression, restlessness and lethargy),
  • Increased vocalization
  • Loss of appetite
  • Weakness
  • Disorientation
  • Paralysis
  • Seizures
  • Sudden death

Diagnosing Rabies

  • There is no accurate test to diagnose rabies in live animals.
  • The direct fluorescent antibody test is the most accurate test for diagnosis, but it can only be performed after the death of the animal.
  • The rabies virus can incubate in a cat’s body anywhere from just one week to more than a year before the virus appears in the saliva and the cat is capable of transmitting the disease.
  • When the animal becomes infectious, symptoms appear quickly. It is possible for a cat, or dog, to shed the virus for several days before clinical signs appear.
  • There is no treatment or cure for rabies once symptoms appear. The disease results in fatality.

What to Do if Your Cat Interacts With a Rabid Animal

  • Put gloves on to protect yourself from infection.
  • Call your veterinarian for an immediate appointment!
  • Contact local animal control officers if the animal who bit your pet is still at large they will be best able to safely apprehend and remove the animal from the environment.
  • A cat who is up to date with his vaccinations and who has been bitten by a possibly rabid animal should also be given a rabies booster vaccine immediately and kept under observation for 45 days.
  • If you think you’ve been bitten by a rabid animal, see your doctor immediately!

Note: Do not attempt to handle or capture a wild animal who is acting strangely (i.e., a nocturnal animal who is out during the day, an animal who acts unusually tame). Report the animal to local animal control officers as soon as possible.


Although the name suggests otherwise, ringworm isn’t caused by a worm at all—but a fungus that can infect the skin, hair and nails. Not uncommon in cats, this highly contagious disease can lead to patchy, circular areas of hair loss with central red rings. Also known as dermatophytosis, ringworm often spreads to other pets in the household—and to humans, too.

Ringworm Symptoms

Classic symptoms of ringworm in cats include:

  • Skin lesions that typically appear on the head, ears and forelimbs.
  • Ringworm can cause flaky bald patches that sometimes look red in the center.
  • In mild cases, there may be localized areas of redness or simply dandruff, while more severe infections can spread over a cat’s entire body.
  • It’s also possible for a pet to carry ringworm spores and not show any symptoms whatsoever.

Ringworm Transmission

A cat can get ringworm directly through contact with an infected animal—or indirectly through contact with bedding, dishes and other materials that have been contaminated with the skin cells or hairs of infected animals. Ringworm spores are notoriously hardy and can survive in the environment for more than a year!

  • Any cat can develop ringworm, but kittens less than a year old and geriatric cats are most prone to infection.
  • Long-haired cats and those who are immunocompromised are also more susceptible.
  • Ringworm can quickly spread in shelters or other crowded environments.
  • Warm and humid conditions tend to promote ringworm infections.

Diagnosing Ringworm

Because infection can potentially spread over a cat’s body, it is important that you see your vet for an accurate diagnosis if you suspect your pet has ringworm. And because the infection can easily spread to you and other animals in the household, it’s a smart idea to immediately quarantine your cat until a veterinarian can confirm a diagnosis. You should also thoroughly wash your hands after you touch your cat.

  • Since some cats show few or no symptoms, a diagnosis of ringworm is rarely made just by looking at the skin.
  • A veterinarian may use an ultraviolet light to diagnose ringworm, or may examine a fungal culture taken from a cat’s hair or skin cells.
  • Skin biopsy and microscopic exam are sometimes also performed.

Treating Ringworm

Treatment of ringworm depends on the severity of the infection.

  • A veterinarian may prescribe a shampoo or ointment that contains a special medication to kill the fungus.
  • In some cases, oral medications are necessary.
  • To ensure that you’ve eradicated this resistant and hardy fungus, treatment may have to be given for several months or more and fungal cultures rechecked periodically.
  • It’s also important to treat the cat’s environment to prevent infection from recurring.

If your veterinarian has diagnosed your cat with ringworm, he or she will explain what you must do to prevent the fungus from spreading to your other pets—and to the human members of the household. But keep in mind that if you have other pets, it’s likely that most of them have been exposed as well. Your veterinarian may recommend that you do the following:

  • Bathe all pets in the household with a medicated rinse or shampoo.
  • Wash the infected animals’ bedding and toys with a disinfectant that kills ringworm spores.
  • Discard items that are impossible to thoroughly disinfect (carpeted cat trees, etc.)
  • Frequently vacuum to rid the house of infected hairs and skin cells. (Yes, the fungus can survive on hair and skin that your cat sheds!)
  • Thoroughly wash your hands after you bathe or touch your cat.

If a cat with ringworm is not properly treated, the lesions can spread over large areas of the animal’s body, causing hair loss and skin infections.

Upper Respiratory Infections

A cat’s upper respiratory tract—the nose, throat and sinus area—is susceptible to infections caused by a variety of viruses and bacteria.

Causes of Upper Respiratory Infections

  • Viruses are the most common causes of upper respiratory infections (URIs) in cats.
  • Feline calicivirus and feline herpesvirus account for 80 to 90% of all contagious upper respiratory problems, and are prevalent in shelters, catteries and multi-cat households.
  • These viruses can be transmitted from cat to cat through sneezing, coughing, or while grooming or sharing food and water bowls.
  • Once infected, cats can become carriers for life, and though they may not show clinical signs, they can still transmit the viruses to others.
  • Cats often develop bacterial infections secondary to these common viral infections.
  • There are also upper respiratory infections in cats that are primarily caused by bacteria. Chlamydia and Bordetella—commonly found in shelters and areas with multiple cats—are two such bacterial infections.
  • Less common in cats than dogs, Bordetella is usually associated with stress and overcrowded living conditions.

Preventing Upper Respiratory Infections

  • Keep your cat indoors to minimize the risk of exposure to infected animals.
  • Properly isolate infected cats to protect other pets living in the same environment.
  • Minimize stress.
  • Keep your cat up to date on vaccines as recommended by your vet. Vaccines for upper respiratory disease in cats may not actually prevent infection, but they help lessen the severity of the disease in some cases.
  • Regular veterinary exams and preventative care can help catch and treat problems early. A cat’s best defense against upper respiratory infection is a healthy immune system.
  • Practice good hygiene and wash your hands thoroughly when handling multiple cats.

Symptoms of Upper Respiratory Infections

Symptoms differ depending on the cause and location of the infection, but some common clinical signs of upper respiratory problems in cats include:

  • Sneezing
  • Congestion
  • Runny nose
  • Cough
  • Clear to colored nasal discharge
  • Gagging, drooling
  • Fever
  • Loss of or decreased appetite
  • Rapid breathing
  • Nasal and oral ulcers
  • Squinting or rubbing eyes
  • Open-mouth breathing
  • Depression

Diagnosing Upper Respiratory Infections

  • Age, vaccination status and physical condition all play a role in a cat’s susceptibility to upper respiratory infections.
  • Cats who live in multi-cat households or shelters are most susceptible.
  • Veterinarians have found that stress plays a role in causing outbreaks of URI, and cats in any shelter, cattery or boarding facility are generally experiencing high levels of stress.
  • Cats who have recovered from URI can become carriers, and may experience recurrences when stressed.
  • Certain breeds like Persians and other flat-faced breeds have a predisposition to develop upper respiratory infections due to their facial structure.

It’s important to bring your cat to a veterinarian if you think she may be suffering from an upper respiratory infection. A brief exam by a veterinarian will help to determine if your cat requires medication, has a fever or is dehydrated. Avoid self-diagnosis, since your cat may be infectious and require isolation, antibiotics or additional veterinary care.

Treating Upper Respiratory Infections

Your veterinarian will prescribe the best course of treatment for your cat, which may include:

  • Medications
  • Isolation
  • Rest
  • Support with fluids
  • Nutritional support

Left untreated, some upper respiratory infections can progress to pneumonia or have other serious complications, such as blindness or chronic breathing difficulties.


Cats can acquire a variety of intestinal parasites, including some that are commonly referred to as “worms.” Infestations of intestinal worms can cause a variety of symptoms. Sometimes cats demonstrate few to no outward signs of infection, and the infestation can go undetected despite being a potentially serious health problem. Some feline parasitic worms are hazards for human health as well.

Common Types of Worms in Cats

Outdoor cats and those who are routinely exposed to soil where other animals defecate are prone to worms. Kittens and cats who do not receive regular preventative health care are most at risk for developing complications associated with internal parasites.

  • Roundworms are the most common internal parasites in cats. Resembling spaghetti, adult worms are three to four inches long. There are several ways cats can become infected. Nursing kittens can get roundworms from an infected mother’s milk, while adult cats can acquire them by ingesting eggs from the feces of an infected cat.
  • Hookworms are much smaller than roundworms—less than an inch long—and reside primarily in the small intestine. Because they feed on an animal’s blood, hookworms can cause life-threatening anemia, especially in kittens. Hookworm eggs are passed in the stool and hatch into larvae, and a cat can become infected either through ingestion or skin contact.
  • Tapeworms are long, flat, segmented parasites that range from 4 to 28 inches in length. An infestation can cause vomiting or weight loss. Cats acquire tapeworms by ingesting an intermediate host, like an infected flea or rodent. When cats are infected, tapeworm segments—actual pieces of the worm that resemble grains of rice—can often be seen on the fur around a cat’s hind end.
  • Lungworms reside in the lungs of a cat. Most cats will not show any signs of having lungworms, but some can develop a cough. Snails and slugs are popular intermediate hosts of this type of parasite, but cats are usually infected after eating a bird or rodent who has ingested an intermediate host.
  • Though means of transmission can vary, one of the main ways that cats get worms is through the ingestion of the feces of infected felines. Mother cats can also pass on worms to their kittens.

Worm Prevention

  • Keep your cat indoors to avoid exposure to infected cats, rodents, fleas and feces.
  • Make sure your home, yard and pets are flea-free.
  • Practice good hygiene and wear gloves when changing cat litter or handling feces. It’s also important to frequently dispose of stool.
  • Ask your veterinarian to recommend an appropriate internal parasite treatment or prevention program for your cat.

Symptoms of Worms in Cats

Symptoms differ depending on the type of parasite and the location of infection, but some common clinical signs include:

  • Diarrhea
  • Worms visible in stool or segments of worm seen near anus
  • Bloody stool
  • Bloating or round, potbellied appearance to abdomen
  • Weight loss
  • Vomiting
  • Constipation
  • Anemia
  • Coughing
  • Trouble breathing

If you think your cat may have worms, it’s important to bring her to a veterinarian, who can confirm the presence of worms. Avoid self-diagnosis, since worms are not always visible or identifiable.

Treatment for Worms

Please don’t attempt to treat your pet yourself—your cat should be treated for the specific type of worms he has.

  • Not all dewormers eradicate all types of worms. Your veterinarian will determine the type of worm(s) infestation(s) your cat has, and prescribe the best course of treatment. Your veterinarian will also be able to tell you if the dewormer should be repeated, and when.
  • Not all dog medications are safe for cats.
  • Some over-the-counter deworming medications can be harmful if used inappropriately.

Transmission of Worms from Cats to Humans

A large number of roundworm eggs can accumulate where cats defecate. People, especially children, who ingest such eggs can develop serious health problems, such as blindness, encephalitis and other organ damage. Treatment of blindness caused by roundworm may involve surgical removal.

Hookworm larvae can penetrate human skin and cause lesions. People can acquire tapeworms through the ingestion of an infected flea, although this is rare.

Australian Population and Hybrids

Australia is home to so many of these animals that they are generally considered pests. A famous “dingo fence” has been erected to protect grazing lands for the continent's herds of sheep. It is likely that more dingoes live in Australia today than when Europeans first arrived.

Though dingoes are numerous, their pure genetic strain is gradually being compromised. They can and do interbreed with domestic dogs to produce hybrid animals. Studies suggest that more than a third of southeastern Australia's dingoes are hybrids.


Morphological Attributes of H. spontaneum

Lines of H. spontaneum that have been introgressed by cultivated germplasm—i.e., feral forms—will appear to be more closely related than others to the H. vulgare gene pool when analyzed molecularly and will thus be erroneously considered as putative progenitors of cultivated barley. To avoid this possibility, a careful morphological analysis is necessary. In this study, 50 of the 367 wild accessions were discarded based on the scoring of the morphological traits described in table 1 . Of those remaining, 207 were collected from primary habitats at known (within 10 km) sampling points. These locations were in Israel and Jordan (group 1 in table 1 also included were four lines collected in southwestern Syria near the border with Jordan), in Lebanon and western Syria (group 3), in the vicinity of Gaza in Turkey (group 4), in the region of Diyarbakir in Turkey and in northern Syria (group 5), in northern Iraq and western Iran (group 6), and in southwestern Iran (group 8). For an additional 66 wild accessions from the Fertile Crescent, only the country of sampling was known (Israel [group 2], Iraq [group 7], or Iran [group 9]). Hordeum spontaneum lines from secondary habitats were included in the groups of Mediterranean and North African origin (group 10) and those from Central Asia (group 11) and the Himalayas (group 12). Group 13 consisted of eight wild accessions of unknown origin. Group 14 contained the 57 cultivated lines of H. vulgare.

Table 1 presents the morphological characterization of the 14 groups of lines considered. Compared with the wild forms, the plants of the cultivated lines were shorter (PH/100), they had larger flag leaves (LW) and ear widths (EW) and shorter glumes (GL), their ears frequently formed six rows (NR), their seeds were broader (SA), and their endosperm grooves were less pronounced (SB/2). The discrimination index had a mean value of 5.30 for the sample of cultivated lines and varied between −0.42 and 1.10 in the 13 groups of wild accessions. Among single wild accessions, the index reached a maximum value of 2.01, while for the group of 20 H. vulgare control lines the minimum value was 3.95. It was concluded that the 317 H. spontaneum accessions selected for molecular fingerprinting did not show evident signs of genetic introgression from H. vulgare. The only exceptions were the four H. spontaneum lines sampled from natural stands in the Himalayan region (group 12): although most of their morphological traits fell within the range of those typical for wild groups, they had ears that virtually lacked awns.

Cultivated Barley is of Monophyletic Origin

Castiglioni et al. (1998) selected from a collection of 5842 accessions 67 H. vulgare lines characterized by large differences in ear, grain, and plant characters and in geographic area of cultivation. The lines were either landraces or old cultivated varieties. Of those lines, 57 were considered in this study. They were cultivated in the Himalayan region (3), in India, Yemen, and Pakistan (5), in Afghanistan, Turkestan, and central Asia (6), in the Mediterranean area (7), in Ethiopia and central Africa (8), in the Balkans (4), in southern Europe (4), in central Europe (8), in northern Europe (5), and in America and Australia (7). The AFLP fingerprinting data for the 57 cultivated lines and the 317 wild accessions were subjected to phylogenetic analyses using different procedures. One tree is reported in figure 4A the 57 cultivated genotypes (red) cluster together, excluding all of the 317 wild accessions (blue). All other trees based on different algorithms gave similar results. This finding allows us to consider the cultivated gene pool as a single taxonomic entity.

Relationships Between Wild and Cultivated Gene Pools

The relationships between groups of wild barley and the cultivated gene pool were assessed based on AFLP allele frequencies calculated for each group of lines. The phylogenetic tree in figure 4B illustrates the position of the cultivated gene pool with respect to six groups of wild lines sampled from precisely known locations within the Fertile Crescent. The wild accessions that are most closely related, as a group, to H. vulgare were sampled in Israel and Jordan. The genetic distances between cultivated and wild groups increase from the southern parts to the northern Fertile Crescent. The lines sampled in southern Iran were, in fact, also closer to cultivated genotypes than were the lines sampled in more northerly locations. Figure 4C shows the result of a similar analysis considering three additional groups of lines also sampled in the Fertile Crescent. Two groups of lines from the Israel and Jordan area—one group sampled at precisely known locations and the second from less well defined areas—map together, both showing the closest relationship with the H. vulgare gene pool. The two Iranian groups also map together, as do the two from Iraq. In figure 4D, wild H. spontaneum lines from secondary habitats were added to the analysis of figure 4B . Lines sampled in Himalayan and Mediterranean locations appeared to be closely related to H. vulgare, while wild lines from central Asia were genetically closer to H. spontaneum genotypes from the eastern part of the Fertile Crescent. The consensus tree in figure 4E indicates that the relationships described in figure 4BD remained almost unchanged when studied with different methods.

A further analysis aimed to localize, within the Israel-Jordan area, sites at which the wild lines are more closely related to the cultivated gene pool. First, the genetic distance between H. vulgare and each of the 317 lines of H. spontaneum was calculated based on the genetic distance DICE ( Dice 1945 ). In this process, the AFLP data for each line were used and compared with a consensus molecular idiotype of H. vulgare. Genetic distances varied between 0.219 and 0.608. An arbitrary group of 45 wild H. spontaneum accessions that appeared to be more closely related to cultivated barley (distance values of between 0.219 and 0.300) was selected. These included, as expected (see Discussion), 9 lines sampled from secondary habitats—4 in the Himalayan region and 5 in Mediterranean locations (1 in Cyrenaica and 4 in Cyprus)—and 34 accessions from the Fertile Crescent. Of the latter, 2 were from Turkey-Northern Syria, 5 were from Iran and 1 was from an unknown sampling point. Of the remaining 26 wild H. spontaneum genotypes from Israel-Jordan, 20 were collected from the sites reported in figure 5A . These 20 lines did not originate from a single geographical area they belong to loose southern (around 33°40′N, 35°15′W) and northern (around 31°45′N, 35°W) clusters.

The relationships between the accessions of the two Israel-Jordan clusters, the five Iranian lines, and the groups of lines sampled in secondary habitats of the Mediterranean and Himalayan regions were also studied with a phylogenetic analysis carried out with AFLP data from single accessions ( fig. 4F ). The tree obtained shows (1) that the Iranian and Israeli lines belong to two separate wild gene pools (2) that the northern and southern Israeli clusters tend to remain separate in this analysis and (3) that the lines from secondary habitats in the Mediterranean are related to the Israeli lines, while the Himalayan accessions are genetically related to the Iranian group of wild lines.

The Himalayan Region as a Center of Cultivated Barley Diversification

The AFLP data indicate the Israel-Jordan area as a possible site of barley domestication (see Discussion). In our AFLP experiments, cultivated landraces were included from other putative centers of barley domestication, such as the Himalayas, Ethiopia, and Morocco. These genotypes unequivocally had a common monophyletic origin with the other cultivated lines analyzed. This excludes the possibility that the regions mentioned were centers of domestication, although they may have been centers of diversification of cultivated barley. This is particularly true for the Himalayan region, where not only local landraces, but also two- and six-rowed wild forms (H. spontaneum and H. agriochriton, respectively) have been sampled.

Mü ller et al. (1995) reported that the barley mutant Hooded (K), a cultivated form introduced to Western countries about 200 years ago from the Himalayan region ( Harlan 1931 ), has a mutation in the homeobox gene BKn-3. Three alleles of the gene were characterized molecularly at the time: wt, K, and K e . The K allele has a 305-bp duplication in intron IV (region C in fig. 2A ). The allele K e has a 33-bp insertion at positions 427–460 in intron IV (region B in fig. 2A ), as well as the duplication of 305 bp. We used the BKn-3 alleles as diagnostic markers to follow the flow of germplasm from wild to cultivated lines. The molecular analysis was also extended to a part of the BKn-3 promoter (region A, positions 1–380 in fig. 2A ).

Regions A, B, and C were sequenced for 12 cultivated barley lines (8 modern Western varieties and 4 lines from the Himalayan region), for 2 H. spontaneum accessions, for a single H. agriocrithon accession from the Himalayas, for 18 K lines, and for 2 K e lines. The three known BKn-3 alleles were detected, as were two new ones ( table 2 ). The two K e lines had allele IIIb, with the 305-bp duplication in region C. BKn-3 alleles from K genotypes were similar to the K e allele but with a deletion of 33 bp in region B (allele IIIc). A line of H. spontaneum and one H. agriocrithon accession from the Himalayan region had allele IIIa. The cultivated Himalayan landraces also had BKn-3 allele IIIa, which can thus be considered the progenitor sequence of K e and K, from which it differs by the absence of the 305-bp duplication. A line of H. spontaneum from Israel had the same allele as the European barley varieties. This allele (allele I) has a deletion of 20 bp at positions 163–182 in region A of the K e sequence and other differences scattered along its DNA sequence. Allele II was found first in the European H. vulgare variety Carina. Its sequence is devoid of the 305-bp duplication and different in several respects from alleles I, IIIa, IIIb, and IIIc ( table 2 ).

Allelic assignment to 320 wild (H. spontaneum and H. agriocrithon) and 109 cultivated Hordeum genotypes—originating from several countries or geographical areas—was completed based on the PCR amplifications described in Materials and Methods. All wt genotypes had alleles that lacked the 305-bp duplication. K e and K lines had, as expected, alleles IIIb and IIIc, respectively. In all of the Hooded lines considered, the 305-bp duplication starts and ends at the same positions. Other PCR amplifications discriminated between wt genotypes that carried alleles I, II, and IIIa.

Table 3 and figure 5B summarize all PCR data concerning BKn-3 allele assignment. In the wild species, the prevailing alleles were II and IIIa. The frequencies of these alleles varied from east to west and from north to south: allele IIIa prevailed in the northeastern part of the Fertile Crescent, while II dominated in southwestern locations. Allele I was rare in wild species and present only in H. spontaneum. The seven instances found were in lines from Israel (6) and Turkey (1). Of the six Israeli-Jordan lines, four were sampled at precise locations ( fig. 5A ).

Among cultivated lines, allele IIIa largely prevailed in the Himalayan region, while allele I was largely dominant among landraces from Europe, Africa, and western Asia. It also prevailed in modern H. vulgare cultivars. In these cultivars, the finding of BKn-3 alleles different from I is easily explained by the use of H. spontaneum in barley breeding as a donor of disease resistance genes ( Nevo 1992 ). Allele IIIb was characteristic for the K e strains, and IIIc was typical for the K genotypes. In summary, allele I, found almost exclusively (but rarely) in the Israel-Jordan region, characterized the wild progenitor which generated, monophyletically, the cultivated Western gene pool of today. In the cultivated barleys of the Himalayas, allele I was replaced by allele IIIa. Allele IIIa in the Himalayan region gave rise to the mutant forms corresponding to genotypes K e and K.


The concrete block building at 3614 Jackson Highway in Sheffield was built around 1946 and was previously a coffin showroom. [6] It was converted to a recording studio in 1969 when a group of musicians called the Muscle Shoals Rhythm Section decided to start their own operation in competition with the FAME Studios owned by Rick Hall. Over the years, artists who recorded at Muscle Shoals Sound Studio included The Rolling Stones, Aretha Franklin, George Michael, Wilson Pickett, Willie Nelson, Lynyrd Skynyrd, Joe Cocker, Levon Helm, Paul Simon, Bob Seger, Rod Stewart, Tamiko Jones, and Cat Stevens. Cher's sixth album was titled 3614 Jackson Highway (1969) and this became the informal name for the studio in 1969. The studio at this location closed in 1979, and the recording facility was moved to new premises at 1000 Alabama Avenue.

The Jackson Highway building had been partly restored and open for tours in 2013 when the documentary Muscle Shoals raised public interest in a major restoration of the studio. [7] The Muscle Shoals Music Foundation was formed in 2013 to raise funds to purchase the building and to complete major renovations. In June 2013, the owner sold the property to the Muscle Shoals Music Foundation, without the historic recording equipment. [8] A large grant from Beats Electronics provided an essential $1 million. The state tourism director said in August 2015 that the 2013 Muscle Shoals film [9] had significant influence. "The financial support from Beats is a direct result of their film." Additional donations were made by other groups and individuals. [10]

As recently as August 2015, tours were visiting the partly restored studio on Jackson Highway. It was closed when major restoration work started in September 2015. Muscle Shoals Sound Studio reopened as a finished tourist attraction on January 9, 2017, owned and operated by the foundation. The interior is reminiscent of the 1970s, with relevant recording equipment and paraphernalia. There are plans to allow artists to record in the studio. [11] [12]

The Alabama Tourism Department named Muscle Shoals Sound Studio as the state's top attraction in 2017, even before the Jackson Highway studio reopened. [4]

Early history Edit

The four founders of the studio, Barry Beckett (keyboards), Roger Hawkins (drums), Jimmy Johnson (guitar) and David Hood (bass), affectionately called The Swampers, [13] but usually known as the Muscle Shoals Rhythm Section, were one of the best-known "house bands" or session musicians. (The nickname "The Swampers" was given to the group by the music producer Denny Cordell during recording sessions for Leon Russell because of their "funky, soulful Southern "swamp" sound".) [14] [2] They are referred to as "The Swampers" in the lyrics of "Sweet Home Alabama" (1974) by Lynyrd Skynyrd and appear on the cover of Cher's 1969 album 3614 Jackson Highway. [15]

Initially they worked for Rick Hall, the founder of FAME Studios and they are recognized as having crafted the "Muscle Shoals sound" in conjunction with Hall. [16] After leaving Rick Hall's FAME Studios, the four musicians partnered with Jerry Wexler who provided start-up funding [17] to found Muscle Shoals Sound Studio at 3614 Jackson Highway in Sheffield. [18] The first hit to the studio's credit was R. B. Greaves' "Take a Letter Maria". By December 1969, the Rolling Stones were recording at this new location for three days. [19]

The Muscle Shoals Rhythm Section was the first group of musicians to own a studio and to eventually run their own publishing and production companies. They provided musical backing and arrangements for many recordings, including major hits by Wilson Pickett, Aretha Franklin, and the Staple Singers a wide range of artists in popular music also recorded hit songs and complete albums at the studio. They had first worked together in 1967 and initially played sessions in New York and Nashville before doing so at FAME. Their initial successes in soul and R&B led to more mainstream rock and pop performers who began coming to record at Muscle Shoals Sound Studios, including the Rolling Stones, Traffic, Bob Seger, Elton John, Boz Scaggs, Willie Nelson, Paul Simon, Bob Dylan, Dr. Hook, Elkie Brooks, Millie Jackson, Julian Lennon, and Glenn Frey.

The two buildings Edit

The studio at 3614 Jackson Highway closed in April 1979, becoming an audio visual retailer and then an appliance store until 1999. The subsequent owner did some renovations and retained the old recording equipment, allowing for tours of the property. [20] [8]

The recording facility was relocated to updated and larger premises at 1000 Alabama Avenue in Sheffield in 1979. This location operated until it was closed and sold in 1985 to Tommy Couch's soul and blues label Malaco Records, based in Jackson, Mississippi, which also bought the publishing rights held by the Muscle Shoals Sound. Malaco used the Sheffield studios for its own artists, including Johnnie Taylor, Bobby Bland and Little Milton, as while continuing to operate its own facility in Jackson. The Rhythm Section, minus Beckett, worked with other studio musicians at Malaco Records and at other studios. [21] In 2005, Couch decided to close the Malaco studio on Alabama Avenue because he was having difficulty competing with more technologically advanced studios. [22]

Recent history Edit

After the 1000 Alabama Avenue location closed in 2005, ending the Muscle Shoals Sound Studio era, the building was taken over by a movie production company. [23] In 2007, this location housed Cypress Moon Productions and the Cypress Moon Studio with functioning recording equipment, which was operating as a recording studio and was open for tours. [24]

Although it was no longer a working studio in 2009 and 2010, the Jackson Highway location was rented for recording some or all of two Grammy-nominated albums. Band of Horses's third CD, Infinite Arms, recorded in part at that studio, was nominated for a Grammy Award in the category Best Alternative Album. [6]

Ten tracks of Black Keys's sixth album, Brothers, were also recorded at 3614 Jackson Highway. [25] The album was nominated for a 2011 Grammy Award for Best Alternative Music Album. Two songs from the album, "Tighten Up" and "Black Mud", were nominated for Grammys: "Tighten Up" for Best Rock Performance by a Duo or Group with Vocal and Best Rock Song and "Black Mud" for Best Rock Instrumental Performance. Rolling Stone magazine placed the album at number-2 on its list of the Best Albums of 2010 and "Everlasting Light" at number 11 on its list of the Best Singles of 2010. The album was also featured on Spin magazine's Top 40 Albums of 2010. [ citation needed ]

The four members of the Muscle Shoals Rhythm Section who had founded the Sound Studio were inducted into the Nashville-based Musicians Hall of Fame in 2008 and into the Alabama Music Hall of Fame in 1995, "as four of the finest studio musicians in the world", also receiving the Lifework Award in 2008. They had appeared on "more than 500 recordings, including 75 gold and platinum hits". [26] [27]

The studio is open for tours Tuesday - Saturday. Over 62,000 people from 50 countries and every state in the U.S. have visited since it opened for tours again in 2013. The studio is a working recording studio at night. Dan Auerbach of the Black Keys did a solo project in March 2017. Grammy winning producer Dave Cobb of Nashville recorded rockers Rival Sons in April 2017. Actor Kiefer Sutherland recorded, along with Swamper David Hood, in May 2017. In 2018, Bishop Gunn released the first recording from the studio after the restoration, "Shine" from their album, Natchez. Donnie Fritz recently released tunes recorded at MSS on his June album, in conjunction with John Paul White and Single Lock Records.

Original studio fate Edit

The original studio building on Jackson Highway was listed on the National Register of Historic Places in June 2006. [28] In June 2013, the building was sold to the Muscle Shoals Music Foundation [29] whose goal was to establish a music museum in the historic building. [30] [31] [32] The foundation extensively restored the building and the studio. It was reopened as a tourist attraction, with plans for recording as well, on January 9, 2017. [4] [33]

According to a journalist who was a recent visitor, the restored studio is impressive: "Muscle Shoals Sound's interior appears much as it did in its prime. . Some guitars and amps. A Hammond organ, Wurlitzer electric piano and black baby grand. The control room with recording console and analog tape machine . There are isolation booths, for vocals, percussion and such. " [34]

Filmmaker Greg Camalier premiered his documentary film Muscle Shoals at the Sundance Film Festival in January 2013. [9] It is about Muscle Shoals sound, and features Rick Hall, FAME Studios, and the Muscle Shoals Rhythm Section (Swampers) who had founded the Muscle Shoals Sound Studios. The film includes interviews with Percy Sledge, Wilson Pickett, Aretha Franklin, Etta James, Mick Jagger, Keith Richards, Steve Winwood, Bono, Alicia Keys and many others.

Watch the video: Photographing a very rare animal: the European wildcat (January 2022).